type stringclasses 1 value | question stringlengths 13 210 | answer stringlengths 5 521 | ideal_answer stringlengths 9 22.1k | documents listlengths 1 133 | snippets listlengths 0 125 | asq_challenge int64 5 13 | folder_name stringclasses 6 values | concepts listlengths 0 23 ⌀ | triples listlengths 0 4.35k ⌀ | id stringlengths 24 24 |
|---|---|---|---|---|---|---|---|---|---|---|
factoid | Which disease can be treated using Tezepelumab? | ['severe asthma'] | ['Tezepelumab can be used to treat severe asthma.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/34572294",
"http://www.ncbi.nlm.nih.gov/pubmed/33368307",
"http://www.ncbi.nlm.nih.gov/pubmed/34572466",
"http://www.ncbi.nlm.nih.gov/pubmed/34606305",
"http://www.ncbi.nlm.nih.gov/pubmed/34608100"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34608100",
"endSection": "abstract",
"offsetInBeginSection": 449,
"offsetInEndSection": 630,
"text": "SUMMARY: Clinical trials demonstrated that tezepelumab, an anti-TSLP monoclonal antibody, is a promising alterna... | 12 | BioASQ-training12b | null | null | 61f7c904882a024a10000027 |
factoid | Chromatin is tightly packed into what structure inside the nucleus? | ['Nucleosome'] | ['Chromatin, a complex of DNA and proteins, is tightly packed into a highly organized structure called the nucleosome inside the nucleus. Nucleosomes are the fundamental repeating units of chromatin and consist of approximately 147 base pairs of DNA wrapped around an octamer of histone proteins, which include two copies each of histone H2A, H2B, H3, and H4. The nucleosomes are connected by linker DNA and further compacted through interactions with additional histone proteins such as histone H1. This organization allows for efficient packaging of the long DNA molecules within the confined space of the nucleus while still permitting access to genetic information for processes like transcription, replication, and repair. The degree of chromatin compaction can vary depending on cellular context and regulatory mechanisms, ultimately influencing gene expression patterns in response to various signals or environmental cues.', 'DNA in eukaryotes is packed into a nucleoprotein complex called chromatin in a manner that enables it to be rapidly accessed during genomic processes. The basic component of chromatin is the nucleosome consisting of DNA wrapped around a histone octamer. Inside the cell nucleus, chromatin is folded into higher-order structures through various mechanisms, including repositioning of nucleosomes along the DNA, packing of nucleosomes into more condensed 3-dimensional configurations, looping of chromatin fibers, and tethering of chromosomal regions to nuclear structures.', 'Chromatin is the complex of DNA and proteins that make up the chromosomes within the nucleus of eukaryotic cells. The basic unit of chromatin is the nucleosome, which consists of DNA wrapped around a histone octamer. Chromatin is folded into higher-order structures through various mechanisms, including repositioning of nucleosomes along the DNA, packing of nucleosomes into more condensed 3-dimensional configurations, looping of chromatin fibers, and tethering of chromosomal regions to nuclear structures. These higher-order structures play important roles in regulating gene expression and other genomic processes. Overall, chromatin provides a means for tightly packaging genetic information while still allowing it to be rapidly accessed during cellular processes.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23109894",
"http://www.ncbi.nlm.nih.gov/pubmed/28058066",
"http://www.ncbi.nlm.nih.gov/pubmed/34255854",
"http://www.ncbi.nlm.nih.gov/pubmed/20444609",
"http://www.ncbi.nlm.nih.gov/pubmed/15868422"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20444609",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 345,
"text": "Our genetic information is tightly packaged into a rather ingenious nucleoprotein complex called chromatin in a ma... | 12 | BioASQ-training12b | null | null | 644ef78f57b1c7a315000084 |
factoid | What is the cause of Facioscapulohumeral Muscular Dystrophy type 2 (FSHD2)? | ['autosomal dominant disease', 'ectopic expression of the transcription factor DUX4 in skeletal muscle', 'mutations in the protein regulating the methylation status of chromatin - SMCHD1'] | ['FSHD2 is caused by mutations in the protein regulating the methylation status of chromatin - SMCHD1.', 'Facioscapulohumeral Muscular Dystrophy type 2 (FSHD2) is an autosomal dominant disease that is caused by the mutations in the protein regulating the methylation status of chromatin - SMCHD1tha leads in the ectopic expression of the transcription factor DUX4 in skeletal muscle.', 'FSHD2 is caused by mutations in the SMCHD1 gene which regulates the methylation status of chromatin.', 'Facioscapulohumeral Muscular Dystrophy type 2 (FSHD2) is caused by mutations in the genes SMCHD1, DNMT3B, and LRIF1.', 'FSHD2 is caused by mutations in the SMCHD1 protein, which regulates the methylation status of chromatin.', 'The cause of FSHD2 is mutations in the protein regulating the methylation status of chromatin - SMCHD1.', 'FSHD2 is caused by mutations in the SMCHD1 gene, which regulates the methylation status of chromatin, affecting the muscle function.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29980640",
"http://www.ncbi.nlm.nih.gov/pubmed/34711481",
"http://www.ncbi.nlm.nih.gov/pubmed/30871534",
"http://www.ncbi.nlm.nih.gov/pubmed/24128691",
"http://www.ncbi.nlm.nih.gov/pubmed/30923442",
"http://www.ncbi.nlm.nih.gov/pubmed/29402602",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30871534",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 212,
"text": "Facial-scapular-humeral myodystrophy Landouzy-Dejerine (FSHD) is an autosomal dominant disease, the basis of its ... | 12 | BioASQ-training12b | null | null | 644298cc57b1c7a315000062 |
factoid | What is the cause of Facioscapulohumeral Muscular Dystrophy type 1 (FSHD1)? | ['autosomal dominant disease', 'partial deletion of the D4Z4 repeats on the 4th chromosome', 'ectopic expression of the transcription factor DUX4 in skeletal muscle'] | ['Facioscapulohumeral muscular dystrophy type 1 (FSHD1) is caused by contraction of the D4Z4 repeat array.', 'Facioscapulohumeral Muscular Dystrophy type 1 (FSHD1) is caused by the loss of DNA repetitive elements (D4Z4 repeats) in the subtelomeric region of chromosome 4q, leading to decreased methylation and epigenetic derepression of the toxic protein DUX4.', 'FSHD1 is an autosomal dominant disease that is caused by partial deletion of the D4Z4 repeats on the 4th chromosome, affecting the expression of DUX4.', 'Facial-scapular-humeral myodystrophy Landouzy-Dejerine (FSHD) is an autosomal dominant disease, the basis of its pathogenesis is ectopic expression of the transcription factor DUX4 in skeletal muscle.', 'FSHD1 is caused by partial deletion of the D4Z4 repeats on the 4th chromosome.', 'The cause of FSHD1 is a partial deletion of the D4Z4 repeats on the 4th chromosome, which affects the expression of DUX4.', 'The cause of Facioscapulohumeral Muscular Dystrophy type 1 (FSHD1) is a partial deletion of the D4Z4 repeats on the 4th chromosome, which affects the expression of DUX4.', 'FSHD1 is caused by a partial deletion of the D4Z4 repeats on chromosome 4.', 'FSHD1 is caused by a partial deletion of D4Z4 repeats on chromosome 4, which affects the expression of the transcription factor DUX4 in skeletal muscle.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31518905",
"http://www.ncbi.nlm.nih.gov/pubmed/14634647",
"http://www.ncbi.nlm.nih.gov/pubmed/24882751",
"http://www.ncbi.nlm.nih.gov/pubmed/30871534",
"http://www.ncbi.nlm.nih.gov/pubmed/27822859",
"http://www.ncbi.nlm.nih.gov/pubmed/24755953",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30871534",
"endSection": "abstract",
"offsetInBeginSection": 213,
"offsetInEndSection": 470,
"text": "There are two types of the disease: FSHD1 (MIM:158900) and FSHD2 (MIM: 158901), which have different genetic cau... | 12 | BioASQ-training12b | null | null | 6442933f57b1c7a315000060 |
factoid | What is CHARMS with respect to medical review of predictive modeling? | ['CHecklist for critical Appraisal and data extraction for systematic Reviews of prediction Modelling Studies (CHARMS).'] | ['CHARMS stands for CHecklist for critical Appraisal and data extraction for systematic Reviews of prediction Modelling Studies (CHARMS).', 'CHARMS stands for Checklist for Critical Appraisal and Data Extraction for Systematic Reviews of Prediction Modeling Studies. It is a tool used to assess the quality of systematic reviews of predictive modeling studies in the medical field.', 'CHecklist for critical Appraisal and data extraction for systematic Reviews of prediction Modelling Studies (CHARMS).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/35321760",
"http://www.ncbi.nlm.nih.gov/pubmed/32978532",
"http://www.ncbi.nlm.nih.gov/pubmed/28284255",
"http://www.ncbi.nlm.nih.gov/pubmed/31439598",
"http://www.ncbi.nlm.nih.gov/pubmed/32453803",
"http://www.ncbi.nlm.nih.gov/pubmed/25314315",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35633976",
"endSection": "abstract",
"offsetInBeginSection": 452,
"offsetInEndSection": 569,
"text": "CHecklist for critical Appraisal and data extraction for systematic Reviews of prediction Modelling Studies (CHA... | 12 | BioASQ-training12b | null | null | 640f857d201352f04a00002b |
factoid | What is the target of Litifilimab? | ['BDCA2'] | ['Litifilimab is a humanized monoclonal antibody against BDCA2 that is being developed for treatment of cutaneous lupus erythematosus.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/35939578",
"http://www.ncbi.nlm.nih.gov/pubmed/36069871"
] | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35939578",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Trial of Anti-BDCA2 Antibody Litifilimab for Cutaneous Lupus Erythematosus."
},
{
"beginSection": "abstract",
... | 12 | BioASQ-training12b | null | null | 63eef3ebf36125a42600000a |
factoid | What is AUROC in context of predictive modeling? | ['area under the receiver operator characteristics curve'] | ['. The area under the receiver operator characteristics curve (AUROC)', "AUROC is an evaluation metric used to measure the performance of a predictive model. It is calculated by measuring the area under the receiver operating characteristic curve, which is a graphical representation of the model's true positive rate and false positive rate.", 'AUROC stands for Area Under the Receiver Operating Characteristic Curve. It is a metric used to evaluate the performance of a predictive model by measuring the trade-off between true positive rate and false positive rate at various threshold levels. A higher AUROC value indicates better model performance.', '. AUROC stands for the area under the receiver operator characteristics curve (AUROC)', 'area under receiver operator curve [AUROC]'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25885260",
"http://www.ncbi.nlm.nih.gov/pubmed/21958955",
"http://www.ncbi.nlm.nih.gov/pubmed/31093546",
"http://www.ncbi.nlm.nih.gov/pubmed/23620757",
"http://www.ncbi.nlm.nih.gov/pubmed/31437918",
"http://www.ncbi.nlm.nih.gov/pubmed/31094792",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35610482",
"endSection": "abstract",
"offsetInBeginSection": 847,
"offsetInEndSection": 915,
"text": ". The area under the receiver operator characteristics curve (AUROC)"
},
{
"beginSection": "abstract",
... | 12 | BioASQ-training12b | null | null | 64136fbf201352f04a00003d |
factoid | When was Keytruda approved by the FDA for the treatment of metastatic non-small cell lung cancer? | ['October 24, 2016'] | ['On October 24, 2016, the U.S. Food and Drug Administration (FDA) approved pembrolizumab (Keytruda) for treatment of metastatic non-small cell lung cancer.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28835513"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28835513",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 713,
"text": "On October 24, 2016, the U.S. Food and Drug Administration (FDA) approved pembrolizumab (Keytruda; Merck & Co., In... | 12 | BioASQ-training12b | null | null | 6415c53e690f196b51000012 |
factoid | What is the estimated reduction in time when using online genetic counseling? | ['8%'] | ['The estimated reduction in the required time through online counseling is about 8%.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26785833"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26785833",
"endSection": "abstract",
"offsetInBeginSection": 1548,
"offsetInEndSection": 1645,
"text": "We estimated reduced time and costs by online counseling with about 8% and 10-12%, respectively. "
}
] | 12 | BioASQ-training12b | null | null | 6415bc8d690f196b5100000f |
factoid | Which company produces Keytruda? | ['Merck & Co., Inc.'] | ['Keytruda is produced by Merck & Co., Inc..'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28835513"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28835513",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 712,
"text": "On October 24, 2016, the U.S. Food and Drug Administration (FDA) approved pembrolizumab (Keytruda; Merck & Co., In... | 12 | BioASQ-training12b | null | null | 6415c599690f196b51000013 |
factoid | Cereblon (CRBN) has been identified as the target for what type of drug? | ['Immunomodulatory drugs (IMiDs)', 'Thalidomide', 'pomalidomide', 'lenalidomide'] | ['Immunomodulatory drugs (IMiDs) thalidomide, lenalidomide, and pomalidomide. IMiDs bind to CRBN and recruit neo-substrates for their ubiquitination and proteasome-mediated degradation', 'Cereblon (CRBN) has been identified as the target for thalidomide and its derivatives such as IMiDs (immunomodulatory drugs).', 'Cereblon (CRBN) has been identified as the target for immunomodulatory and antiproliferative activities of lenalidomide and pomalidomide.', 'Cereblon (CRBN) has been identified as the target for immunomodulatory drugs (IMiDs) such as thalidomide, lenalidomide, and pomalidomide.', 'Cereblon (CRBN) has been identified as the target for thalidomide and its derivatives, known as immunomodulatory drugs (IMiDs), such as lenalidomide and pomalidomide.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33777938",
"http://www.ncbi.nlm.nih.gov/pubmed/26990986",
"http://www.ncbi.nlm.nih.gov/pubmed/26186254",
"http://www.ncbi.nlm.nih.gov/pubmed/26002965",
"http://www.ncbi.nlm.nih.gov/pubmed/34316334",
"http://www.ncbi.nlm.nih.gov/pubmed/21207098",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36252444",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 195,
"text": "Cereblon is a well-known target of thalidomide and its derivatives."
},
{
"beginSection": "abstract",
... | 12 | BioASQ-training12b | null | null | 6414638c201352f04a000047 |
factoid | What is the difference between dermatillomania and skin picking disorder? | ['None'] | ['Dermatillomania is also known as skin picking disorder (SPD).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33808008"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33808008",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 241,
"text": "Dermatillomania or skin picking disorder (SPD) is a chronic, recurrent, and treatment resistant neuropsychiatric d... | 12 | BioASQ-training12b | null | null | 6414c4cf690f196b51000006 |
factoid | What causes Japanese Spotted Fever? | ['Rickettsia japonica'] | ['Japanese Spotted Fever is caused by Rickettsia japonica.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/35507925",
"http://www.ncbi.nlm.nih.gov/pubmed/36016429",
"http://www.ncbi.nlm.nih.gov/pubmed/32863353"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32863353",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "Non-pathogenic Rickettsia species LON strains closely related to an agent of Japanese spotted fever (JSF), R. japo... | 12 | BioASQ-training12b | null | null | 63eefa3bf36125a426000012 |
factoid | Olokizumab is tested for which disease? | ['rheumatoid arthritis'] | ['Olokizumab, a monoclonal antibody against interleukin 6, improves outcomes of rheumatoid arthritis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/34344706",
"http://www.ncbi.nlm.nih.gov/pubmed/36001712"
] | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34344706",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "Olokizumab, a monoclonal antibody against interleukin 6, in combination with methotrexate in patients with rheumatoid ar... | 12 | BioASQ-training12b | null | null | 63eef60ef36125a42600000c |
factoid | What disease can be treated with Lenacapavir? | ['HIV-1'] | ['Lenacapavir is a long-acting, highly potent HIV-1 capsid (CA) inhibitor that is approved for treatment of HIV-1.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36272024",
"http://www.ncbi.nlm.nih.gov/pubmed/34871187",
"http://www.ncbi.nlm.nih.gov/pubmed/36190128",
"http://www.ncbi.nlm.nih.gov/pubmed/36202818"
] | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36190128",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Structural and Mechanistic Bases of Viral Resistance to HIV-1 Capsid Inhibitor Lenacapavir."
},
{
"beginSection":... | 12 | BioASQ-training12b | null | null | 63f03fc8f36125a426000021 |
factoid | What cells proliferate in Mantle Cell Lymphoma | ['B cells'] | ["Mantle cell lymphoma is a subtype of B-cell non-Hodgkin's lymphoma, where B-cells proliferate uncontrollably.", 'Mantle Cell Lymphoma is characterized by the proliferation of mantle cells, which are a type of B-cell lymphocytes.', 'Mantle Cell lymphoma is an aggressive (fast-growing) type of B-cell non-Hodgkin lymphoma', "Mantle cell lymphoma (MCL) is a subtype of B-cell non-Hodgkin's lymphoma seen predominantly in males.", 'Mantle cell lymphoma is a type of B-cell non-Hodgkin lymphoma characterized by the proliferation of malignant B-cells in the mantle zone of the lymph node.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33197439",
"http://www.ncbi.nlm.nih.gov/pubmed/22555177",
"http://www.ncbi.nlm.nih.gov/pubmed/8277026",
"http://www.ncbi.nlm.nih.gov/pubmed/10463985",
"http://www.ncbi.nlm.nih.gov/pubmed/10942246",
"http://www.ncbi.nlm.nih.gov/pubmed/8649059",
"http://www.ncbi.nlm.nih... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32774275",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Mantle cell lymphoma (MCL) is a relatively rare B-cell non-Hodgkin lymphoma, typically presenting with extensive l... | 12 | BioASQ-training12b | null | null | 640c85e9201352f04a000026 |
factoid | What is the estimated cost reduction when using telegenetics? | ['10-12%'] | ['The estimated cost reduction by online counseling is about 10-12%.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26785833"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26785833",
"endSection": "abstract",
"offsetInBeginSection": 1548,
"offsetInEndSection": 1644,
"text": "We estimated reduced time and costs by online counseling with about 8% and 10-12%, respectively."
}
] | 12 | BioASQ-training12b | null | null | 6415bb3c690f196b5100000e |
factoid | What is the target of BI 1015550? | ['phosphodiesterase 4B'] | ['BI 1015550 is a preferential phosphodiesterase 4B inhibitor that is used for patients with idiopathic pulmonary fibrosis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/35569036",
"http://www.ncbi.nlm.nih.gov/pubmed/35517783",
"http://www.ncbi.nlm.nih.gov/pubmed/36299369"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35569036",
"endSection": "abstract",
"offsetInBeginSection": 181,
"offsetInEndSection": 402,
"text": "METHODS: In this phase 2, double-blind, placebo-controlled trial, we investigated the efficacy and safety of BI ... | 12 | BioASQ-training12b | null | null | 63f03ae6f36125a42600001d |
factoid | Beremagene Geperpavec is tested for which disease? | ['recessive dystrophic epidermolysis bullosa'] | ['Beremagene Geperpavec was tested for recessive dystrophic epidermolysis bullosa.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/35347281"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35347281",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 393,
"text": "Recessive dystrophic epidermolysis bullosa (RDEB) is a lifelong genodermatosis associated with blistering, woundin... | 12 | BioASQ-training12b | null | null | 63eeeaaaf36125a426000004 |
factoid | Hairpatches is a single gene mutation associated with what disease? | ['alopecia and renal failure'] | ['Hairpatches is a single gene mutation associated with progressive renal failure and alopecia in mice, and may be a potential model for a newly described heritable human disorder.', 'Hairpatches is a single gene mutation associated with progressive renal disease and alopecia.', 'Hairpatches is a single gene mutation characterized by progressive renal disease and alopecia in the mouse', 'Hairpatches, a single gene mutation characterized by progressive renal disease and alopecia in the mouse. A potential model for a newly described heritable human disorder.', '"Hairpatches" (Hpt) is a naturally occurring, autosomal semi-dominant mouse mutation. Hpt/Hpt homozygotes die in utero, while Hpt/+ heterozygotes exhibit progressive renal failure accompanied by patchy alopecia.', '"Hairpatches" (Hpt) is a naturally occurring, autosomal semi-dominant mouse mutation. Hairpatches, a single gene mutation characterized by progressive renal disease and alopecia in the mouse.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23301070",
"http://www.ncbi.nlm.nih.gov/pubmed/1836514"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23301070",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "\"Hairpatches\" (Hpt) is a naturally occurring, autosomal semi-dominant mouse mutation. Hpt/Hpt homozygotes die in... | 12 | BioASQ-training12b | null | null | 64138ce8201352f04a000042 |
factoid | What is the alternative microexon splicing by RBFOX2 and PTBP1 associated with? | ['colorectal cancer metastasis'] | ['Alternative microexon splicing by RBFOX2 and PTBP1 is associated with metastasis in colorectal cancer'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36394206",
"http://www.ncbi.nlm.nih.gov/pubmed/34346508"
] | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36394206",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Alternative splicing of HSPA12A pre-RNA by SRSF11 contributes to metastasis potential of colorectal cancer."
},
{
... | 12 | BioASQ-training12b | null | null | 63f9cd0b33942b094c000010 |
factoid | Which gene is implicated in Canavan disease? | ['ASPA'] | ['Canavan disease is an inherited leukodystrophy resulting from mutations in the gene encoding aspartoacylase (ASPA).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36267868",
"http://www.ncbi.nlm.nih.gov/pubmed/35636725",
"http://www.ncbi.nlm.nih.gov/pubmed/35637731",
"http://www.ncbi.nlm.nih.gov/pubmed/35929936"
] | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36267868",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Cribriform Appearance of White Matter in Canavan Disease Associated with Novel Mutations of ASPA Gene."
},
{
"be... | 12 | BioASQ-training12b | null | null | 63f56f7533942b094c000002 |
factoid | What disease can be treated with Glofitamab? | ['DLBCL'] | ['Glofitamab is being tested for treatment of DLBCL after CAR T-Cell Therapy'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/35626120",
"http://www.ncbi.nlm.nih.gov/pubmed/34941996",
"http://www.ncbi.nlm.nih.gov/pubmed/36198538"
] | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35626120",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "Glofitamab Treatment in Relapsed or Refractory DLBCL after CAR T-Cell Therapy."
},
{
"beginSection": "abstract",
... | 12 | BioASQ-training12b | null | null | 63eeeb70f36125a426000005 |
factoid | Which molecule is targeted by upadacitinib? | ['Janus kinase 1'] | ['Upadacitinib is a Janus kinase 1 inhibitor under development for the treatment of several inflammatory disorders including rheumatoid arthritis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28503781",
"http://www.ncbi.nlm.nih.gov/pubmed/29908670",
"http://www.ncbi.nlm.nih.gov/pubmed/30500075",
"http://www.ncbi.nlm.nih.gov/pubmed/29672874",
"http://www.ncbi.nlm.nih.gov/pubmed/29688617",
"http://www.ncbi.nlm.nih.gov/pubmed/28765121",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28765121",
"endSection": "abstract",
"offsetInBeginSection": 1255,
"offsetInEndSection": 1554,
"text": "We summarise the development and recent application of Janus kinase (JAK) inhibitors in the treatment of IMIDs... | 8 | BioASQ-training8b | null | null | 5c7039207c78d69471000065 |
factoid | What type of extracolonic tumors does the PMS2 germline mutation cause? | ['endometrial cancer', 'ovarian cancer', 'gastric cancer', 'small bowell cancer', 'ureter cancer', 'urothelial cancers'] | ['The PMS2 gene is one of the mismatch repair genes that play a crucial role in maintaining genomic stability. Germline mutations in the PMS2 gene can lead to Lynch syndrome, which is an autosomal dominant disorder characterized by an increased risk of developing colorectal and other types of cancer. However, compared to other MMR genes such as MLH1 and MSH2, PMS2 germline mutations are less common and associated with a lower risk of cancer development. , Extracolonic tumors associated with PMS2 germline mutations include endometrial, gastric, small bowel, biliary tract, pancreatic, brain (usually glioblastoma), sebaceous skin tumors, and transitional cell carcinomas of the ureter and renal pelvis. However, it is important to note that the risk of developing extracolonic tumors in individuals with PMS2 mutations is lower than in those with MLH1 or MSH2 mutations. , It is also worth mentioning that PMS2 germline mutations have be', 'PMS2 is one of the four DNA mismatch repair proteins, which plays a significant role in maintaining genomic stability. PMS2 germline mutation results in Lynch syndrome, which predisposes to various extracolonic tumors, including endometrial, ovarian, gastric, and urothelial cancers.', 'The PMS2 germline mutation causes extracolonic tumors, including endometrial cancer and colorectal and endometrial cancer.', "Lynch syndrome, which can be caused by PMS2 germline mutations, predisposes to various extracolonic cancers including endometrial cancer, ovarian cancer, stomach cancer, renal pelvis and ureteral cancer, small bowel cancer, hepatobiliary tract cancer, pancreatic cancer, glioblastoma multiforme (in Turcot's variant), sebaceous skin tumors (in Muir-Torre variant), and more recently identified, breast and prostate cancers.", 'The PMS2 germline mutation does not cause any extracolonic tumors.', 'The PMS2 germline mutation causes a severe colorectal cancer and multiple adenoma phenotype without extraintestinal cancer. The patient presented with multiple gastrointestinal tumors, which could not be distinguished clinically from cases with attenuated familial adenomatous polyposis or MUTYH-associated polyposis. In addition, the cumulative incidence of extracolonic tumors was higher in females than males (p = 0.001), including uterus and breast cancers. However, path_MLH1 variants are significantly more associated with the development of colorectal cancer than extracolonic tumors, while path_MSH2 variants show a greater frequency of extracolonic cancers, including ovarian cancer.', 'PMS2 is a mismatch repair gene that plays a critical role in maintaining genomic integrity. A germline mutation in PMS2 is associated with Lynch syndrome (also known as hereditary nonpolyposis colorectal cancer syndrome). This mutation increases the risk of colorectal cancer and other extracolonic malignancies such as endometrial, ovarian, gastric, small bowel, pancreatic, ureter, and renal pelvis cancer', 'The PMS2 germline mutation is associated with a slightly increased risk for colorectal and endometrial cancer. However, it does not appear to increase the risk for any other types of cancer associated with Lynch syndrome.', 'Based on the provided abstract, a study was conducted to determine the age-specific cumulative risk (penetrance) of various cancers for carriers of heterozygous pathogenic PMS2 variants. The research involved a large dataset from a global collaboration and used modified segregation analysis while considering both genotyped and nongenotyped relatives. , The results showed that PMS2 mutation carriers had an increased risk for colorectal cancer and endometrial cancer compared to the general population. However, there was no clear evidence of an elevated risk for ovarian, gastric, hepatobiliary, bladder, renal, brain, breast, prostate, or small bowel cancer. , In conclusion, the PMS2 germline mutation primarily causes an increased risk for colorectal and endometrial cancers. The study did not find a significant association between PMS2 germline mutations and other Lynch syndrome-associated extracolonic tumors.', 'The PMS2 germline mutation is associated with an increased risk of developing various extracolonic malignancies, including but not limited to endometrial cancer, ovarian cancer, stomach cancer, small intestine cancer, hepatobiliary tract cancers (liver and bile duct), urinary tract tumors (kidney and ureter), brain tumors such as gliomas, skin cancers like melanoma, and pancreas cancer. The exact spectrum of extracolonic tumors can vary among different studies and populations, but these are the most commonly reported types associated with PMS2 mutations.', 'PMS2 is a gene associated with Lynch syndrome, which is a hereditary predisposition to colorectal and extracolonic cancers. The extracolonic tumors associated with PMS2 germline mutation include gynecologic (endometrial and ovarian), urologic (urinary tract and renal pelvis), small bowel, pancreas, stomach, biliary tract, and skin (sebaceous neoplasms).', 'The PMS2 germline mutation is predominantly associated with colorectal and endometrial cancer within the Lynch tumor spectrum. However, there is no clear evidence of an increased risk of other extracolonic tumors such as ovarian, gastric, hepatobiliary, bladder, renal, brain, breast, prostate, or small bowel cancer.', 'The PMS2 germline mutation can cause several extracolonic tumors. These include cancers of the ovary, stomach, liver and biliary system, bladder, kidney, brain, breast, and prostate, as well as small bowel cancer. It is essential to monitor individuals with PMS2 mutations closely for these potential malignancies.', 'The PMS2 germline mutation is associated with an increased risk of developing extracolonic tumors, specifically endometrial cancer.', 'PMS2 germline mutation causes extracolonic tumors in regions such as the endometrium, ovary, urinary tract, lymphoma, stomach, pancreas small bowel and brain.', 'Germline mutations of the PMS2 gene are associated with an increased risk of colorectal cancer in individuals with hereditary nonpolyposis colorectal cancer (HNPCC) syndrome. However, PMS2 germline mutations are rarely associated with extracolonic tumors in familial aggregation of colorectal cancers.', 'The PMS2 germline mutation is associated with a slightly increased risk for colorectal and endometrial cancer. However, it does not appear to increase the risk for any other types of cancer associated with Lynch syndrome. Lynch syndrome is a genetic disorder that increases the risk of many types of cancer, particularly cancers of the colon (colorectal cancer) and endometrium.', 'Heterozygous PMS2 mutation carriers were at small increased risk for colorectal and endometrial cancer but not for any other Lynch syndrome-associated cancer.', 'The PMS2 germline mutation leads to café-au-lait macules, colonic polyps, and a unique range of tumors.', 'The PMS2 germline mutation is associated with an increased risk of colorectal and endometrial cancer, but not with other Lynch syndrome-associated cancers. Heterozygous PMS2 mutation carriers have a small increased risk for colorectal and endometrial cancer. However, the mutation does not seem to increase the risk of other extracolonic tumors. Therefore, the answer is that PMS2 germline mutation causes colorectal and endometrial cancer, but not other Lynch syndrome-associated cancers.', 'The PMS2 germline mutation is associated with an increased risk of developing colorectal cancers (CRCs) that differ from sporadic CRCs in genetic and histologic features. In addition, tumors from patients with PMS2-associated Lynch syndrome have been found to be distinct from colorectal tumors associated with defects in other mismatch repair genes. , However, the PMS2 germline mutation does not cause extracolonic tumors, such as brain tumors, haematological malignancies, and signs of neurofibromatosis type 1, which are more commonly associated with biallelic MMR gene mutations. , In summary, the PMS2 germline mutation is primarily linked to the development of colorectal cancers with unique genetic and histological features, whereas extracolonic tumors are more frequently observed in individuals with biallelic MMR gene mutations.', 'PMS2 germline mutations are associated with an increased risk of extracolonic tumors, including tumors in regions such as the endometrium, ovary, urinary tract, lymphoma, stomach, pancreas, small bowel, and brain in individuals with Lynch Syndrome.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29758216",
"http://www.ncbi.nlm.nih.gov/pubmed/18602922",
"http://www.ncbi.nlm.nih.gov/pubmed/18273873",
"http://www.ncbi.nlm.nih.gov/pubmed/19132747",
"http://www.ncbi.nlm.nih.gov/pubmed/30161022",
"http://www.ncbi.nlm.nih.gov/pubmed/31056861",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30161022",
"endSection": "abstract",
"offsetInBeginSection": 1516,
"offsetInEndSection": 1675,
"text": "Heterozygous PMS2 mutation carriers were at small increased risk for colorectal and endometrial cancer but not... | 13 | BioASQ-training13b | null | null | 65f7736fc4010b4d78000024 |
factoid | What proportion of risk is attributable to obesity in colorectal cancer women development? | ['Hazard Ratio 1.04', '4%', 'HR 1.04 (1.01-1.18) p<0.001'] | ['In women, obesity is associated with a 16% increased risk of developing colorectal cancer. This means that approximately 16% of the risk of colorectal cancer in women can be attributed to obesity.', 'The hazard ratio for colon cancer risk in obese women is 1.04 [1.01-1.18], indicating a slight increase in risk associated with obesity.', 'The proportion of risk attributable to obesity in the development of colorectal cancer among women is 1.04 (95% CI: 1.01-1.18).', 'The proportion of risk attributable to obesity in colorectal cancer women development is 1.20 for each 0.1-unit increase in waist-hip ratio.', '1.04 [1.01-1.18]', 'In women, colon cancer risk increased by 16% per 10-cm increase in waist circumference (RR: 1.16; 95% CI: 1.09, 1.23) and by 20% per 0.1-unit increase in waist-hip ratio (RR: 1.20; 95% CI: 1.08, 1.33). Obese women had a 4% higher risk of colon cancer compared to non-obese women (hazard ratio = 1.04; 95% CI: 1.01-1.18).', 'The population attributable fraction (PAF) for obesity in colorectal cancer in women is 9%.', 'The proportion of risk attributable to obesity in colorectal cancer development in women is approximately 1.13-1.17 times that of men.', '”BMI and/or the number of CTCs were significantly associated with the risk of CRC (P values of less than 0.001 for all). The proportion of risk attributable to BIM was 31% (95% confidence interval: 27% to 35%). The proportion of risk attributable to the number of CTCs was 49% (95% confidence interval: 43% to 55%).”}</s>', 'The men in the obese/obese group had a higher risk of colon cancer than women (hazard ratio\u2009=\u20091.13 [1.10-1.17] in men, and hazard ratio\u2009=\u20091.04 [1.01-1.18] in women, P\u2009=\u20090.001).', "The specific proportion of risk attributable to obesity in colorectal cancer development in women is not explicitly stated in the provided snippets. However, it is indicated that an increase in waist circumference and waist-hip ratio is associated with an increased risk of colon cancer in women. For every 10-cm increase in waist circumference, the relative risk (RR) increases by 1.16. Similarly, for every 0.1-unit increase in waist-hip ratio, the RR increases by 1.20. Furthermore, women in the obese group had a hazard ratio of 1.04 for colon cancer, indicating a slightly increased risk compared to non-obese women. It's important to note that the association between obesity and colon and rectal cancer risk varies by sex and cancer site", "The exact proportion of risk attributable to obesity in colorectal cancer development in women is not specified in the provided documents. However, they do provide relative risk (RR) values for increases in waist circumference and waist-hip ratio, which are measures often associated with obesity. For every 10-cm increase in waist circumference, the RR is 1.16, and for every 0.1-unit increase in waist-hip ratio, the RR is 1.20. Additionally, the hazard ratio for colon cancer in obese women is 1.04, suggesting that obesity increases the risk of colon cancer in women by 4%. It's important to note that these are not direct measures of the proportion of risk attributable to obesity, but rather indications of the relative risk compared to non-obese individuals.", 'The exact percentage may vary, but providing an approximate range or qualitative description would be helpful. The study found that approximately 10-25% of colorectal cancer cases in women are attributable to obesity.', 'The risk of colon cancer increased with increasing waist circumference (per 10-cm increase) in both men (RR: 1.33; 95% CI: 1.19, 1.49) and women (RR: 1.16; 95% CI: 1.09, 1.23) and with increasing waist-hip ratio (per 0.1-unit increase) in both men (RR: 1.43; 95% CI: 1.19, 1.71) and women (RR: 1.20; 95% CI: 1.08, 1.33). The men in the obese/obese group had a higher risk of colon cancer than women (hazard ratio\\u2009=\\u20091.13 [1.10-1.17] in men, and hazard ratio\\u2009=\\u20091.04 [1.01-1.18] in women, P\\u2009=\\u20090.001).', 'According to the provided information, the proportion of colorectal cancer risk attributable to obesity in women varies by population:\n\n- In Italian women, a decrease in waist-to-hip ratio below 0.82 might reduce colorectal cancer by 19%.\n\n- In Pacific women, the population attributable fraction (PAF) for obesity was 19%. \n\n- In Maori women, the PAF for obesity was 14%.\n\n- In European/other women, the PAF for obesity was 8%.\n\nOverall, obesity increases the risk of colorectal cancer in women by around 19%, but this varies from 8-19% depending on the specific population. The relative risk is estimated to be about 1.5 times higher in obese women compared to normal-weight women.', 'According to the study, the proportion of risk attributable to obesity in colorectal cancer women development is 1.04 (hazard ratio) [1.01-1.18] in women, which means that obesity increases the risk of colorectal cancer in women by 4% (1.04-1.00) compared to non-obese women. This suggests that obesity plays a role in the development of colorectal cancer in women, but the effect size is relatively small compared to other risk factors.', 'Obesity increases the risk of developing colorectal cancer in women by a factor ranging from 1.04 to 1.18.', 'Obesity contributes to an increased risk of colorectal cancer development in women, with a hazard ratio of 1.04 to 1.18. This indicates that a proportion of the risk of colon cancer in women can be attributed to obesity.', 'The proportion of risk attributable to obesity in colorectal cancer development in women varies depending on the cancer site. For colon cancer, a 5-unit increase in body mass index (BMI) is associated with a 12% increased risk in women. However, for rectal cancer, there is a weak or no association between BMI and risk in women. Therefore, the proportion of risk attributable to obesity in colorectal cancer development in women is higher for colon cancer compared to rectal cancer.', 'According to the provided snippets, the risk of colon cancer in women is associated with increasing waist circumference and waist-hip ratio, with a higher risk observed in men compared to women. Specifically, the hazard ratio for colon cancer in women was found to be 1.04 (95% CI: 1.01-1.18) per 10-cm increase in waist circumference, and 1.20 (95% CI: 1.08-1.33) per 0.1-unit increase in waist-hip ratio. However, the proportion of risk attributable to obesity in colorectal cancer women development is not explicitly stated in the provided snippets. , Therefore, we cannot provide a specific proportion of risk attributable to obesity in colorectal cancer women development based on the given information. However, it is clear that obesity is a significant risk factor for colon cancer in both men and women, and that the association between obesity and colon cancer risk varies by sex and cancer site.', "The exact proportion of colorectal cancer risk that is attributable to obesity can vary depending on the study and the population being considered. However, research has consistently shown that there is a positive association between excess body weight and an increased risk of developing colorectal cancer, particularly in women. Studies have estimated that approximately 3-5% of all colorectal cancers may be attributable to obesity among women. It's important to note that these estimates are based on observational studies and can fluctuate due to factors such as study design, sample size, and the specific measures used to define obesity.", 'In women, 1.04 times higher risk of colorectal cancer development is attributable to obesity.', '16% of risk of colorectal cancer in women development is attributable to obesity.', 'The study found that approximately 15.8% of the total costs in obesity-related cancers among women can be reduced, with a significant portion of this reduction coming from post-menopausal breast, liver, and colorectal cancers. However, the study does not provide a specific proportion of risk attributable to obesity in colorectal cancer women development.', 'The population attributable fractions (PAFs) for excess weight were 24.3% for colon and 18.9% for rectum among women. This means that approximately 24.3% of colon cancer cases and 18.9% of rectum cancer cases in women are attributable to obesity.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/19207714",
"http://www.ncbi.nlm.nih.gov/pubmed/27196525",
"http://www.ncbi.nlm.nih.gov/pubmed/30448606",
"http://www.ncbi.nlm.nih.gov/pubmed/37264099",
"http://www.ncbi.nlm.nih.gov/pubmed/12117878",
"http://www.ncbi.nlm.nih.gov/pubmed/20843489",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17823417",
"endSection": "abstract",
"offsetInBeginSection": 1166,
"offsetInEndSection": 1586,
"text": "Colon cancer risk increased with increasing waist circumference (per 10-cm increase) in both men (RR: 1.33; 95... | 13 | BioASQ-training13b | null | null | 65f7728fc4010b4d78000021 |
factoid | What is the relationship between Electroporation (EP) and DNA vaccines? | ['increase immunogenicity of the vaccine'] | ['Yes, electroporation is an effective way to increase the immunogenicity of DNA.', 'Electroporation (EP) is used to enhance the effectiveness of DNA vaccines by increasing their immunogenicity. This means it helps to boost the immune response triggered by the DNA vaccines.', 'Electroporation (EP) is a method of delivering DNA vaccines that significantly increases transfection efficacy and the subsequent vaccine-specific immune responses.', 'Electroporation (EP) is an effective way to increase the immunogenicity of DNA vaccines.', 'Electroporation (EP) is an effective way to increase the immunogenicity of DNA vaccines. EP is used to deliver plasmid DNA vaccines, enhancing the immune response induced by the vaccine.', 'Electroporation (EP) is a physical method used to facilitate the entry of DNA vaccines (plasmid DNA molecules) into cells, significantly improving their efficacy by inducing humoral and cellular immune responses by over 400- and 35-fold respectively.', 'Electroporation (EP) is a method that increases the immunogenicity of DNA vaccines, particularly plasmid DNA vaccines.', 'Electroporation (EP) is a method that has been shown to significantly augment the transfection efficacy and the subsequent vaccine-specific immune responses of DNA vaccines.', 'Electroporation (EP) is an effective way to increase the DNA vaccines immunogenicity.', 'Electroporation (EP) increases the immunogenicity of DNA vaccines.', 'Electroporation (EP) effectively enhances the immunogenicity of DNA vaccines.', 'Electroporation allows efficient delivery of DNA into cells and tissues, improving the expression of therapeutic or immunogenic proteins that are encoded by plasmid DNA, which is used in DNA vaccines.', 'Electroporation (EP) is a technique used to increase the immunogenicity of DNA vaccines. It involves the use of an electric field to create temporary pores in the cell membrane, allowing the DNA to enter the cell and be expressed as antigens, which can stimulate an immune response.', 'Electroporation (EP) is a method used to increase the immunogenicity of DNA vaccines.', 'Electroporation (EP) is an effective way to increase the immunogenicity of plasmid DNA vaccine.', 'Electroporation (EP) is associated with increasing the immunogenicity of DNA vaccines.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21180650",
"http://www.ncbi.nlm.nih.gov/pubmed/36992261",
"http://www.ncbi.nlm.nih.gov/pubmed/22284894",
"http://www.ncbi.nlm.nih.gov/pubmed/38034030",
"http://www.ncbi.nlm.nih.gov/pubmed/23684840",
"http://www.ncbi.nlm.nih.gov/pubmed/15110305",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38063059",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 260,
"text": "Electroporation (EP) is an effective way to increase the immunogenicity of DNA"
},
{
"beginSection": "ab... | 13 | BioASQ-training13b | null | null | 65f494d7c4010b4d78000013 |
factoid | What type of DMD can golodirsen be used for? | ['exon 53'] | ['Golodirsen can be used to treat Duchenne muscular dystrophy (DMD) patients who have a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Golodirsen is approved for the treatment of DMD in patients who have a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Patients with a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Golodirsen (Vyondys 53™) is an antisense oligonucleotide designed to induce exon 53 skipping in patients with Duchenne muscular dystrophy (DMD) who have a confirmed mutation of the DMD gene that is amenable to this specific form of therapy.', 'Golodirsen can be used for the treatment of DMD in patients with a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Golodirsen can be used for the treatment of Duchenne muscular dystrophy (DMD) in patients with a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Golodirsen is a drug that can be used for the treatment of Duchenne muscular dystrophy (DMD) in patients with a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Golodirsen is used for treating Duchenne muscular dystrophy that can benefit from exon 53 skipping.', 'Golodirsen can be used for Duchenne muscular dystrophy (DMD) in patients with a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Golodirsen is approved for the treatment of DMD in patients with a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Golodirsen is approved by the FDA for the treatment of Duchenne Muscular Dystrophy (DMD) patients who are amenable to exon 53 skipping.', 'Golodirsen (Vyondys 53™) can be used for treating Duchenne muscular dystrophy (DMD) in patients with a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Golodirsen is used for treating DMD in patients who have a specific mutation that can be treated by skipping exon 53.', 'Golodirsen (Vyondys 53™) is approved for the treatment of Duchenne muscular dystrophy (DMD) in patients with a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Golodirsen can be used for the treatment of Duchenne Muscular Dystrophy (DMD) in patients who have a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Golodirsen (VYONDYS 53TM) can be used for specific types of Duchenne Muscular Dystrophy (DMD) that are amenable to exon 53 skipping.', 'Golodirsen can be used for DMD with a confirmed mutation amenable to exon 53 skipping.', 'Golodirsen can be used for Duchenne muscular dystrophy (DMD) patients who are amenable to exon 53 skipping.', 'Golodirsen can be used for Duchenne muscular dystrophy (DMD) with a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.', 'Golodirsen (Vyondys 53™) can be used for the treatment of Duchenne muscular dystrophy (DMD) in patients with a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/32139505",
"http://www.ncbi.nlm.nih.gov/pubmed/36401027",
"http://www.ncbi.nlm.nih.gov/pubmed/34092651",
"http://www.ncbi.nlm.nih.gov/pubmed/32026421",
"http://www.ncbi.nlm.nih.gov/pubmed/33407808",
"http://www.ncbi.nlm.nih.gov/pubmed/34788571",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32026421",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Golodirsen (Vyondys 53™), an antisense oligonucleotide of the phophorodiamidate morpholino oligomer (PMO) subclass... | 13 | BioASQ-training13b | null | null | 64179034690f196b5100002b |
factoid | What proportion of alteration in NTRK genes are attributable to colorectal cancer? | ['Less than 0.5%', '0.5%'] | ['The proportion of alterations in NTRK genes attributable to colorectal cancer is relatively low, with NTRK gene fusions occurring in approximately 1% of colorectal cancer cases.', 'The rate of alterations in NTRK genes among common cancers is generally below 0.5%, with rare morphological subtypes, colorerectal microsatellite instability (MSI) tumors, and driver mutation exclusion cancers having higher rates. Colorectal cancer specifically has been found to have a higher prevalence of NTRK gene alterations compared to other common cancers, although the exact rate can vary depending on factors such as MSI status and the presence or absence of certain driver mutations.', 'In colorectal cancer, the proportion of alterations in NTRK genes is consistently below 0.5%. However, rare morphological subtypes, colorectal microsatellite instability, and driver mutation exclusion cancers show higher rates of alterations in NTRK genes.', 'The proportion of alteration in NTRK genes attributable to colorectal cancer is not well established in the literature. However, it is known that NTRK gene alterations are relatively rare in colorectal cancer, occurring in approximately 1-3% of cases. Therefore, the proportion of alteration in NTRK genes attributable to colorectal cancer is likely to be small.', 'In common cancers, rates were consistently below 0.5%. Rare morphological subtypes, colorectal microsatellite instability, and driver mutation exclusion cancers had higher rates.', 'The proportion of alteration in NTRK genes attributable to colorectal cancer is 0.0001%.', 'Alterations in NTRK genes attributable to colorectal cancer account for 0.5% of cases, with higher rates observed in rare morphological subtypes and those with microsatellite instability.', 'The prevalence of NTRK gene fusions in colorectal cancer is generally low, ranging from approximately 0.23% to 0.7% in most studies. However, one study found a higher prevalence of around 7% specifically in the microsatellite instability-high (MSI-high) colorectal cancer subgroup.', 'The proportion of alterations in NTRK genes attributable to colorectal cancer is consistently below 0.5%. However, it is important to note that rare morphological subtypes, colorectal microsatellite instability, and driver mutation exclusion cancers may have higher rates of NTRK gene alterations.', 'The text does not provide specific information on the proportion of alteration in NTRK genes attributable to colorectal cancer. It mentions that common cancers have rates consistently below 0.5%, and that rare morphological subtypes, colorectal microsatellite instability, and driver mutation exclusion cancers have higher rates. However, it does not specify the rate for colorectal cancer or NTRK gene alterations.', 'The proportion of alterations in NTRK genes attributable to colorectal cancer is below 0.5%.', 'The proportion of alteration in NTRK genes attributable to colorectal cancer (CRC) is around 10% in the pan-cancer population, and 0.2% of CRCs (9/4569) were positive for Pan-Trk IHC. Additionally, the prevalence of NTRK fusion in CRC was 0.18%, with 46 unique NTRK-fusion partner pairs, of which 33 were not previously reported. TRK positivity was observed in 19% of MLH1-methylated MSI-high CRCs, 17% of sessile serrated lesions with dysplasia (SSLDs), and 4% of sessile serrated lesions (SSLs). However, NTRK gene alterations are not enriched in gastric cancer (GC) with dMMR but are specifically enriched in cases of GAHED.', "Based on the information provided in the snippet, it is not possible to directly determine the proportion of alterations in NTRK genes that are attributable to colorectal cancer. The snippet discusses the rates of cancers in general and mentions rare morphological subtypes, microsatellite instability, and driver mutation exclusion cancers having higher rates, but it does not provide specific details about NTRK gene alterations or their association with colorectal cancer. , However, it is known that NTRK gene fusions can occur across various tumor types, including colorectal cancer, but they are considered rare events. According to a study published in Cancer Discovery, the frequency of NTRK gene fusions in colorectal cancer is estimated to be around 0.18-0.23% (Cancer Discov. 2017 Aug;7(8):824-836). , Therefore, while it's challenging to provide an exact proportion based on the given snippet, it can be inferred that alterations in NTRK genes attributable to colorectal cancer are relatively rare events.", 'According to the literature review, NTRK gene fusions are found in approximately 0.2% to 0.3% of colorectal cancers. This means that out of every 100 colorectal cancers, 2 to 3 cases will have an NTRK gene fusion. Therefore, the proportion of alterations in NTRK genes attributable to colorectal cancer is relatively low, but still significant enough to consider testing for these fusions in certain subgroups of patients.', '0.25% of patients analyzed had NTRK gene fusions and the most common were breast cancer, colorectal cancer (CRC), and sarcoma.', 'According to the systematic review, the proportion of NTRK gene fusions attributable to colorectal cancer is not specifically stated. However, it is mentioned that rare morphological subtypes, such as colorectal microsatellite instability, and driver mutation exclusion cancers have higher rates of NTRK fusions. The review also notes that the prevalence of NTRK fusions in common cancers, including colorectal cancer, is consistently below 0.5%. Therefore, it can be inferred that the proportion of NTRK alterations attributable to colorectal cancer is likely low, but further large-scale, standardized genomic data are needed to characterize NTRK fusion epidemiology in this specific cancer type.', 'The exact proportion of NTRK gene alterations attributable to colorectal cancer (CRC) is not provided in the text. However, the text does mention that NTRK gene fusions are found in approximately 0.16-0.3% of CRCs and that they are more frequent in MMR-deficient/BRAFV600E wild-type tumors (5.3%). Additionally, the study found that 7% of MSI-high CRC cohort had NTRK gene fusions. It is important to note that these frequencies are based on specific patient populations and may not be generalizable to all patients with CRC.', 'In common cancers, rates of NTRK gene alterations were consistently below 0.5%. Rare morphological subtypes, colorectal microsatellite instability, and driver mutation exclusion cancers had higher rates.', "According to the provided text, approximately 7% of colorectal cancers (CRCs) have NTRK gene fusions. This means that about 7% of alterations in NTRK genes are attributable to CRC. However, it's important to note that not all NTRK alterations are necessarily driver mutations or functional, and some may be passengers or non-pathogenic variants. Therefore, the actual proportion of NTRK alterations that contribute to the development and progression of CRC is likely lower than 7%.", 'The rates of NTRK gene alterations were consistently below 0.5% in common cancers. However, colorectal cancers with microsatellite instability had higher rates of NTRK alterations compared to common cancers overall.', 'Rates of NTRK gene alteration were consistently below 0.5% in common cancers, but in rare morphological subtypes and colorectal microsatellite instability, and driver mutation exclusion cancers, higher rates of NTRK gene alteration were reported.', 'Alterations in NTRK genes attributable to colorectal cancer account for approximately 0.5% and are associated with colorectal microsatellite instability.', 'Approximately less than 0.5% of alterations in NTRK genes are associated with colorectal cancer. NTRK gene fusions have been identified as oncogenic drivers across various tumor types; however, they are relatively rare in colorectal cancer, making up a very small proportion of genetic changes observed in this cancer type.', '0.5% or less.', 'The proportion of alteration in NTRK genes attributable to colorectal cancer is below 0.5%.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/34402529",
"http://www.ncbi.nlm.nih.gov/pubmed/36914665",
"http://www.ncbi.nlm.nih.gov/pubmed/31567189",
"http://www.ncbi.nlm.nih.gov/pubmed/36041373",
"http://www.ncbi.nlm.nih.gov/pubmed/36077692",
"http://www.ncbi.nlm.nih.gov/pubmed/28174090"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36914665",
"endSection": "abstract",
"offsetInBeginSection": 975,
"offsetInEndSection": 1154,
"text": " In common cancers, rates were consistently below 0.5%. Rare morphological subtypes, colorectal microsatellite ... | 13 | BioASQ-training13b | null | null | 65f77397c4010b4d78000025 |
factoid | Cilta-cel was developed for treatment of which disease? | ['multiple myeloma'] | ['Cilta-cel, a BCMA-targeting chimeric antigen receptor T-cell therapy for multiple myeloma.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37014590",
"http://www.ncbi.nlm.nih.gov/pubmed/34175021",
"http://www.ncbi.nlm.nih.gov/pubmed/37716872",
"http://www.ncbi.nlm.nih.gov/pubmed/37913909",
"http://www.ncbi.nlm.nih.gov/pubmed/37497629",
"http://www.ncbi.nlm.nih.gov/pubmed/36271807",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36411210",
"endSection": "abstract",
"offsetInBeginSection": 1174,
"offsetInEndSection": 1407,
"text": " Additional indirect treatment comparisons conducted separately for ide-cel and cilta-cel have demonstrated th... | 13 | BioASQ-training13b | null | null | 65cfd4b21930410b13000020 |
factoid | What is the main cause of spillover events? | ['The main cause of spillover events is the disruption of habitats of the reservoir species.', 'The main cause of spillover events is the interface between humans, wildlife, and domesticated animals, which is associated with high habitat fragmentation, biodiversity loss through land use change, high livestock densities, agricultural inputs, and wildlife hunting.'] | ['The main cause of spillover events is the interaction between wildlife, domestic animals, and humans, often influenced by factors such as habitat loss, agricultural practices, and land use for food production. Spillover events occur when pathogens are transmitted from one species to another, leading to potential outbreaks of zoonotic diseases. Factors like habitat destruction and encroachment into wildlife areas can increase the risk of spillover events, highlighting the importance of understanding and managing these interactions to prevent disease transmission.', 'The main cause of spillover events is the disruption of habitats of the reservoir species.', 'The main causes of spillover events include human land modification, domestication, horizontal gene transfer, microbial succession, climate change, biodiversity loss, and globalization.', 'The main cause of spillover events and emerging infectious diseases is cross-species transmission of pathogens, particularly from animals to humans (zoonoses). Key drivers that facilitate this process include:\n\n1. Increased contact and sharing of space between wildlife, humans, and domesticated animals, often due to human intrusion into natural habitats.\n\n2. Agricultural intensification, animal trade, and certain herd management practices.\n\n3. High mutation and recombination rates in some viruses (e.g., coronaviruses) that enable host jumping and adaptation to new species.\n\n4. Specific human behaviors, such as hunting, butchering, and consuming wild animal meat, especially in hotspots like bushmeat markets.\n\n5. Domestication of wild animals as pets or for other purposes, bringing them into close proximity with humans.\n\nIn summary, the growing human-animal interface, coupled with the ability of some pathogens to adapt to new hosts, is the key driver of zoonotic spillover events.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29466832",
"http://www.ncbi.nlm.nih.gov/pubmed/37019573",
"http://www.ncbi.nlm.nih.gov/pubmed/33052311",
"http://www.ncbi.nlm.nih.gov/pubmed/37007505",
"http://www.ncbi.nlm.nih.gov/pubmed/37000877"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37019573",
"endSection": "abstract",
"offsetInBeginSection": 925,
"offsetInEndSection": 1161,
"text": "the extent of land use for food production and the agricultural practices employed that shape four archetypal f... | 13 | BioASQ-training13b | null | null | 65f8447fc4010b4d78000043 |
factoid | What is the cause of Leigh syndrome? | ['pyruvate dehydrogenase complex, and respiratory chain complexes I, II, III, IV, V defects', 'defects of mitochondrial enzyme complexes', 'mitochondrial DNA mutations', 'nuclear DNA mutations'] | ['Leigh syndrome may result from several defects of mitochondrial enzyme complexes, including pyruvate dehydrogenase complex, and respiratory chain complexes I, II, III, IV, V.', 'Leigh syndrome is caused by defects in mitochondrial enzyme complexes. These can include the pyruvate dehydrogenase complex, and respiratory chain complexes I, II, III, IV, and V.', 'Leigh syndrome is caused by various genetic defects, including m.9185T>C MTATP6 variant, Surf1 gene mutations, G8363A mitochondrial DNA mutation, deficiencies in the FAO enzyme short-chain enoyl-CoA hydratase 1 (ECHS1) and defects of 16 mitochondrial DNA (mtDNA) genes and approaching 100 nuclear genes.', 'Leigh syndrome is a severe neurological disorder caused by defects in several mitochondrial enzyme complexes. These include the pyruvate dehydrogenase complex and respiratory chain complexes I, II, III, IV, and V. Additionally, complex V deficiency associated with the NARP point mutation and cytochrome c oxidase deficiency can also lead to Leigh syndrome.', 'Leigh syndrome can result from various defects in mitochondrial enzyme complexes, including pyruvate dehydrogenase complex deficiency, respiratory chain complexes I, II, III, IV, and V deficiencies. Specifically, it can be caused by defects in pyruvate dehydrogenase complex, cytochrome c oxidase deficiency, complex I deficiency, and complex V deficiency associated with the NARP point mutation.', 'Leigh syndrome may result from several defects of mitochondrial enzyme complexes, including pyruvate dehydrogenase complex deficiency, cytochrome c oxidase deficiency, complex I deficiency, complex II deficiency, complex III deficiency, complex IV deficiency, and complex V deficiency associated with the NARP point mutation.', 'Leigh syndrome may result from different enzyme defects, most notably pyruvate dehydrogenase complex deficiency, cytochrome c oxidase deficiency, complex I deficiency, and complex V deficiency associated with the recently described NARP point mutation.', 'Leigh syndrome is caused by various genetic mutations that affect mitochondrial function, leading to impaired energy production and neurodegeneration. These mutations can involve genes related to mitochondrial DNA or nuclear DNA, resulting in deficiencies in oxidative phosphorylation and the accumulation of toxic metabolites. The exact cause of Leigh syndrome can vary among individuals, with over 110 different genes implicated in its development.', 'Leigh syndrome is caused by several defects of mitochondrial enzyme complexes, including pyruvate dehydrogenase complex, and respiratory chain complexes I, II, III, IV, V.', 'Leigh syndrome is caused by defects in mitochondrial enzyme complexes, including pyruvate dehydrogenase complex deficiency, cytochrome c oxidase deficiency, complex I deficiency, complex V deficiency, and the NARP point mutation.', 'The cause of Leigh syndrome is a result of different enzyme defects, most notably pyruvate dehydrogenase complex deficiency, cytochrome c oxidase deficiency, complex I deficiency, and complex V deficiency associated with the recently described NARP point mutation.', 'Leigh syndrome is a rare inherited neurometabolic disorder. It is caused by several defects of mitochondrial enzyme complexes, including pyruvate dehydrogenase complex, and respiratory chain complexes I, II, III, IV, V.', 'Leigh syndrome is a genetically heterogeneous neurodegenerative disorder caused by mutations in nuclear genes or mitochondrial DNA that impair mitochondrial energy metabolism. Over 75 different causative gene mutations have been identified, with approximately 75% being nuclear DNA mutations and 25% mitochondrial DNA mutations. These mutations affect various components of the mitochondrial respiratory chain complexes, pyruvate metabolism, vitamin and cofactor transport and metabolism, mtDNA maintenance, mitochondrial gene expression, protein quality control, lipid remodeling, dynamics, and toxicity.', 'Leigh syndrome may result from several defects of mitochondrial enzyme complexes, including pyruvate dehydrogenase complex.', 'Leigh syndrome can be caused by several defects of mitochondrial enzyme complexes, including pyruvate dehydrogenase complex, respiratory chain complexes I, II, III, IV, and V. Additionally, it can also be caused by cytochrome c oxidase deficiency, complex I deficiency, and complex V deficiency associated with the NARP point mutation.', 'Leigh syndrome is caused by defects in mitochondrial enzyme complexes, including pyruvate dehydrogenase complex, respiratory chain complexes I, II, III, IV, V, and the recently described NARP point mutation.', 'Leigh syndrome can result from defects in mitochondrial enzyme complexes, including pyruvate dehydrogenase complex, and respiratory chain complexes I, II, III, IV, and V. Deficiencies in enzymes such as pyruvate dehydrogenase complex, cytochrome c oxidase, complex I, and complex V can contribute to the development of Leigh syndrome.', 'Leigh syndrome may result from different enzyme defects, most notably pyruvate dehydrogenase complex deficiency, cytochrome c oxidase deficiency, complex I deficiency, and complex V deficiency.', 'Leigh syndrome may result from different enzyme defects, most notably pyruvate dehydrogenase complex deficiency, cytochrome c oxidase deficiency, and complex I deficiency.', 'Leigh syndrome can be caused by defects in mitochondrial enzyme complexes, including deficiencies in pyruvate dehydrogenase complex, cytochrome c oxidase, complex I, and complex V, as well as mutations like the NARP point mutation.', 'Leigh syndrome can be caused by defects in mitochondrial enzyme complexes, such as pyruvate dehydrogenase complex deficiency and respiratory chain complexes I, II, III, IV, V.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/19046652",
"http://www.ncbi.nlm.nih.gov/pubmed/16023078",
"http://www.ncbi.nlm.nih.gov/pubmed/10443880",
"http://www.ncbi.nlm.nih.gov/pubmed/12943968",
"http://www.ncbi.nlm.nih.gov/pubmed/26657515",
"http://www.ncbi.nlm.nih.gov/pubmed/29512743",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18651330",
"endSection": "abstract",
"offsetInBeginSection": 281,
"offsetInEndSection": 443,
"text": "It may result from several defects of mitochondrial enzyme complexes, including pyruvate dehydrogenase complex, ... | 13 | BioASQ-training13b | null | null | 6451007857b1c7a315000093 |
factoid | What is the indication for Alirocumab? | ['high cholesterol', 'hypercholestoremia'] | ['Alirocumab is primarily used to lower LDL-cholesterol levels.', 'Alirocumab is indicated for the prevention of cardiovascular risk, and for patients with heterozygous familial hypercholesterolemia, atherosclerotic cardiovascular disease, or hypercholesterolemia who require additional LDL-C lowering.', 'Alirocumab is a fully human immunoglobulin G1 monoclonal antibody directed against proprotein convertase subtilisin/kexin type 9 (PCSK9) approved for the treatment of hypercholesterolemia in high-risk patients.', 'Alirocumab is indicated for the treatment of hypercholesterolaemic patients unable to meet LDL-C targets, as an adjunct to diet in addition/alternative to LLT.', 'Alirocumab is a PCSK9 inhibitor that is used to decrease LDL-cholesterol levels in patients who have not been able to achieve target levels with other treatments. It is approved for clinical use by European regulatory authorities.', 'The indication for Alirocumab is lowering LDL cholesterol levels.', 'Alirocumab is indicated for cholesterol and triglyceride metabolism, acting on them.', 'Alirocumab is used for treatment of low-density lipoprotein cholesterol.', 'The indication for Alirocumab is for patients who have high cardiovascular risk from established atherosclerotic cardiovascular disease or heterozygous familial hypercholesterolemia and who are unable to achieve LDL-C targets with maximally tolerated dose of statins with or without other lipid-lowering drugs.', 'Alirocumab is indicated for the treatment of hypertriglyceridemia.', 'Alirocumab is an anti-PCSK9 monoclonal antibody that is used for the treatment of high cholesterol.', 'Alirocumab is indicated for the treatment of hypercholesterolemia.', 'Alirocumab is indicated for the treatment of adults with heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease who require additional lowering of LDL-cholesterol.', 'Alirocumab, sold under the brand name Praluent, is a medication used as a second-line treatment for high cholesterol for adults whose cholesterol is not controlled by diet and statin treatment', 'Alirocumab is indicated for the treatment of hypercholesterolemia in high-risk patients, heterozygous familial hypercholesterolemia, and clinical atherosclerotic cardiovascular disease where low-density lipoprotein cholesterol (LDLC) lowering is insufficient.', 'Alirocumab is indicated for the treatment of hypertriglyceridemia in adults with established cardiovascular disease or diabetes mellitus type 2 and mixed dyslipidemia.', 'The indication for Alirocumab is to reduce LDL cholesterol levels in patients who have not achieved their target LDL cholesterol levels with maximally tolerated statin therapy or in patients who are intolerant to statins.', 'The indication for Alirocumab is to reduce LDL-cholesterol and triglyceride metabolism.', 'Alirocumab is indicated for LDL-cholesterol reduction.', 'Alirocumab is indicated for the reduction of low-density lipoprotein cholesterol (LDL-cholesterol), particularly in patients who have not been able to achieve target LDL-cholesterol levels with traditional treatments.', 'Alirocumab is a PCSK9 inhibitor indicated for lowering LDL cholesterol. It is used in patients who cannot achieve target LDL cholesterol levels with other lipid-lowering therapies.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26563849",
"http://www.ncbi.nlm.nih.gov/pubmed/26785741",
"http://www.ncbi.nlm.nih.gov/pubmed/26935836",
"http://www.ncbi.nlm.nih.gov/pubmed/26859553",
"http://www.ncbi.nlm.nih.gov/pubmed/26886466",
"http://www.ncbi.nlm.nih.gov/pubmed/29802110",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35052871",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 49,
"text": "Effects of Alirocumab on Triglyceride Metabolism:"
},
{
"beginSection": "abstract",
"document": "http://www.n... | 13 | BioASQ-training13b | null | null | 65f70b9cc4010b4d7800001c |
factoid | What disease can be treated with Tebentafusp? | ['uveal melanoma'] | ['Tebentafusp is approved for uveal melanoma.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37141553",
"http://www.ncbi.nlm.nih.gov/pubmed/37650713",
"http://www.ncbi.nlm.nih.gov/pubmed/37207136",
"http://www.ncbi.nlm.nih.gov/pubmed/36970111",
"http://www.ncbi.nlm.nih.gov/pubmed/36229663",
"http://www.ncbi.nlm.nih.gov/pubmed/37444540",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37444540",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Tebentafusp in Patients with Metastatic Uveal Melanoma: A Real-Life Retrospective Multicenter Study."
},
{
"begi... | 13 | BioASQ-training13b | null | null | 65cec1fb1930410b13000005 |
factoid | When was Havana Syndrome first recognized? | ['2016'] | ['Havana Syndrome is the name given to the group of neurological symptoms that first occurred among the staff at the U.S. embassy in Havana, Cuba in 2016.', 'Havana syndrome is a term that was first coined by US diplomats and intelligence personnel in 2016 in Havana, Cuba, to describe a series of strange symptoms, including dizziness, hearing loss, headaches, and cognitive impairment.', 'Havana Syndrome was first recognized in late 2016 when U.S. diplomatic personnel in Havana, Cuba, reported experiencing unusual symptoms including hearing loss, cognitive issues, and other neurological problems.', 'Havana Syndrome was first recognized in 2016.', 'In 2016, Havana Syndrome was first recognized when U.S. diplomats serving in Havana, Cuba reported hearing strange noises accompanied by a constellation of unexplained health effects.', 'Havana Syndrome is a term used to describe a series of unexplained neurological symptoms experienced by diplomatic personnel serving in Havana, Cuba, beginning in 2016.', 'Since 2016, an array of claims and public discourse have circulated in the medical community over the origin and nature of a mysterious condition dubbed "Havana Syndrome," so named as it was first identified in Cuba.', 'The Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba reported hearing strange noises accompanied by a constellation of unexplained health effects.', 'Havana Syndrome was first recognized in Havana, Cuba in late 2016 when several U.S. diplomats and embassy staff reported experiencing unexplained neurological symptoms.', 'Havana Syndrome was first recognized in 2016 when diplomatic personnel serving in Havana, Cuba, reported audible sensory phenomena paired with complex and persistent neurological symptoms consistent with brain injury.', 'Havana Syndrome was first recognized in the year 2016.', ' Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba reported hearing strange noises accompanied by a constellation of unexplained health effects.', 'Havana Syndrome was first recognized in late 2016 when several U.S. diplomats stationed in Havana, Cuba, reported experiencing a range of unexplained neurological symptoms.', 'Havana Syndrome was first recognized in 2016 when diplomatic personnel in Havana, Cuba reported experiencing unusual sensory phenomena and neurological symptoms.', 'Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba reported hearing strange noises accompanied by a constellation of unexplained health effects.', 'Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba began reporting audible sensory phenomena paired with onset of complex and persistent neurological symptoms consistent with brain injury.', 'Havana Syndrome was first recognized in 2016 when diplomatic personnel serving in Havana, Cuba reported audible sensory phenomena paired with complex and persistent neurological symptoms consistent with brain injury.', 'In 2016 diplomatic personnel serving in Havana, Cuba began reporting audible sensory phenomena paired with onset of complex and persistent neurological symptoms consistent with brain injury.', 'Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba reported hearing strange noises and experiencing unexplained health effects.', 'Havana syndrome is a term used to describe a cluster of neurological symptoms that have been reported by United States and Canadian diplomats, intelligence officers, and other government employees, mainly in Havana, Cuba, between 2016 and 2018.', 'The phenomenon now known as Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba reported hearing strange noises accompanied by a constellation of unexplained health effects.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37965360",
"http://www.ncbi.nlm.nih.gov/pubmed/32655474",
"http://www.ncbi.nlm.nih.gov/pubmed/30828629",
"http://www.ncbi.nlm.nih.gov/pubmed/35962646",
"http://www.ncbi.nlm.nih.gov/pubmed/37976420"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37965360",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 206,
"text": " In 2016 diplomatic personnel serving in Havana, Cuba, began reporting audible sensory phenomena paired with onse... | 13 | BioASQ-training13b | null | null | 65f856a1c4010b4d7800004e |
factoid | Which age group should never be tested for HIV infection? | ['None.'] | ['There is no age group that should never be tested for HIV infection. HIV testing is recommended for all individuals, regardless of age, as early detection and treatment can improve outcomes and prevent transmission.', 'There is no specific age group that should never be tested for HIV infection. Early testing and diagnosis is crucial for effective treatment and prevention of HIV transmission.', 'No age group should be excluded from HIV testing. Early diagnosis and treatment are crucial in managing HIV infection and preventing its spread. Testing for HIV should be encouraged for all individuals, regardless of age, to ensure timely intervention and appropriate care.', 'There is no age group that should never be tested for HIV infection.', 'There is no age group that should never be tested for HIV infection. The CDC recommends that all adults, adolescents, and pregnant women in health-care settings be offered HIV testing, and that those at high risk for HIV infection be tested at least annually. Additionally, the WHO recommends that all people aged 15-64 years should be offered an HIV test at least once in their lifetime. It is important to note that anyone can be at risk for HIV infection regardless of age, gender, or sexual orientation.', "There is no age group that should never be tested for HIV infection. HIV can affect individuals of all ages, from newborns to older adults. In fact, late diagnosis of HIV is a significant issue, particularly among older individuals, heterosexuals, and non-Europeans. Therefore, it's crucial to get tested regardless of age to ensure early detection and treatment. This can help reduce the burden of late presentation and advanced disease", 'There is no age group that should never be tested for HIV infection. Testing for HIV is important for everyone, regardless of age, to ensure early detection and appropriate care.', 'There is no age group that should never be tested for HIV infection. In fact, the World Health Organization recommends that all people aged 15-64 years old get tested for HIV at least once in their lifetime, and those at high risk of infection get tested annually. Children born to mothers living with HIV also need to be tested regularly as they are at a higher risk of acquiring the virus through mother-to-child transmission. Early diagnosis and treatment of HIV can significantly improve health outcomes and reduce the risk of transmission. Therefore, it is important for all individuals, regardless of age, to know their HIV status and take appropriate measures to protect themselves and their partners.', 'There is no specific age group that should never be tested for HIV infection. HIV testing is recommended for everyone, regardless of age, as early diagnosis and treatment can help prevent the progression of the disease and reduce the risk of transmission to others.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37993765",
"http://www.ncbi.nlm.nih.gov/pubmed/36629794",
"http://www.ncbi.nlm.nih.gov/pubmed/19940800",
"http://www.ncbi.nlm.nih.gov/pubmed/28796758",
"http://www.ncbi.nlm.nih.gov/pubmed/9611559",
"http://www.ncbi.nlm.nih.gov/pubmed/12126721",
"http://www.ncbi.nlm.ni... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34949518",
"endSection": "abstract",
"offsetInBeginSection": 293,
"offsetInEndSection": 410,
"text": "social and clinical inequalities of more children infected with HIV and more children losing their fight against... | 13 | BioASQ-training13b | null | null | 65f86ba3c4010b4d78000059 |
factoid | What does capnography measure? | ['Carbon dioxide', 'Co2', 'end-tidal carbon dioxide (EtCO2)'] | ['Capnography measures the amount of carbon dioxide in exhaled air, indicating how well CO2 is being eliminated from the body.', 'Capnography measures the amount of carbon dioxide (CO2) in exhaled breath.', 'Capnography is a tool for continuous monitoring of carbon dioxide (CO2) concentration in exhaled gases during anesthesia and respiratory support.', 'Capnography measures carbon dioxide in expired air.', 'Capnography measures the concentration of carbon dioxide at the end of exhalation, and it can detect abnormal breathing patterns or the absence of breath.', 'Capnography is a non-invasive monitoring technique that measures the concentration or partial pressure of carbon dioxide (CO2) in exhaled breath, also known as end-tidal CO2 (EtCO2), over time to assess the adequacy of ventilation and the presence of abnormal ventilation or apnea.', 'Capnography measures carbon dioxide concentration in exhaled air.', 'Capnography is a monitoring tool used in medicine that measures the concentration of carbon dioxide in the respiratory gases. It is often used during cardiopulmonary resuscitation to measure arterial CO2 partial pressure (PCO2). Additionally, it is used for monitoring end-tidal carbon dioxide concentrations.', 'Capnography measures end-tidal carbon dioxide concentrations, which can detect abnormal ventilation or apnoea early during cardiopulmonary resuscitation.', 'Capnography measures the amount of carbon dioxide in expired air.', 'Capnography measures the concentration of carbon dioxide in exhaled air.', 'Capnography is the measurement of carbon dioxide (CO2) concentration in a gas mixture.', 'Capnography measures the end-tidal carbon dioxide (CO2) concentration in exhaled breath. It provides a non-invasive and continuous assessment of ventilation and can detect abnormal ventilation or apnea early during cardiopulmonary resuscitation.', 'Capnography measures the concentration of carbon dioxide in the respiratory gases, which is a vital parameter during anesthesia and intensive care. It is used to monitor the inhaled and exhaled concentration or partial pressure of carbon dioxide. This can help detect abnormal ventilation or apnoea early', 'Capnography measures carbon dioxide, volumetric capnography (VCAP) and arterial CO2 partial pressure, and arterial CO2 partial pressure.', "Capnography measures the concentration of carbon dioxide (CO2) in exhaled breath. It provides real-time monitoring of the patient's ventilation and helps assess the adequacy of respiratory function.", 'Capnography measures the concentration of carbon dioxide (CO2) in exhaled breath as a function of time, known as the capnogram.', "Capnography measures end-tidal carbon dioxide concentrations. This means it monitors the amount of carbon dioxide that is exhaled at the end of each breath. It's a useful tool because it can detect abnormal ventilation or apnoea early.", 'Capnography measures the concentration of carbon dioxide in exhaled breath, which can be used to monitor the effectiveness of cardiopulmonary resuscitation.', 'Capnography provides real-time measurement of carbon dioxide (CO2) in respiratory gases.', 'Capnography measures the concentration of carbon dioxide in the respiratory gases, specifically the end-tidal carbon dioxide concentrations. It is used to monitor the inhaled and exhaled concentration or partial pressure of carbon dioxide.', 'Capnography measures end-tidal carbon dioxide (CO2) concentrations during respiration. It can detect abnormal ventilation or apnea by monitoring CO2 levels in exhaled breath.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/18156957",
"http://www.ncbi.nlm.nih.gov/pubmed/26264607",
"http://www.ncbi.nlm.nih.gov/pubmed/7736268",
"http://www.ncbi.nlm.nih.gov/pubmed/24785676",
"http://www.ncbi.nlm.nih.gov/pubmed/2511789",
"http://www.ncbi.nlm.nih.gov/pubmed/26714621",
"http://www.ncbi.nlm.nih... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37507472",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "A secondary analysis of a randomized study was performed to study the relationship between volumetric capnography ... | 13 | BioASQ-training13b | null | null | 65f38059c4010b4d7800000e |
factoid | What is the target of Selpercatinib? | ['rearranged during transfection (RET) kinase'] | ['Selpercatinib is an orally-administered, selective inhibitor of rearranged during transfection (RET) kinase approved for the treatment of advanced RET fusion-positive non-small cell lung cancer (NSCLC).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37265026",
"http://www.ncbi.nlm.nih.gov/pubmed/36122315",
"http://www.ncbi.nlm.nih.gov/pubmed/32703767",
"http://www.ncbi.nlm.nih.gov/pubmed/32493697",
"http://www.ncbi.nlm.nih.gov/pubmed/37718634",
"http://www.ncbi.nlm.nih.gov/pubmed/37070927",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36729098",
"endSection": "abstract",
"offsetInBeginSection": 359,
"offsetInEndSection": 486,
"text": "More recently, two selective RET inhibitors, selpercatinib and pralsetinib, demonstrated higher efficacy and goo... | 13 | BioASQ-training13b | null | null | 65cfa22b1930410b1300000c |
factoid | What is the vector for coxiella burnetii transmission? | ['tick'] | ['The vector for Coxiella burnetii transmission is primarily through inhalation of infectious aerosols, although ticks have also been suggested as potential vectors.', 'Coxiella burnetii is transmitted by ticks, including through their feces and saliva.', 'The vector for Coxiella burnetii transmission is the tick.', 'The vector for Coxiella burnetii transmission is ticks.', 'Coxiella burnetii is transmitted by ticks.', 'The vector for Coxiella burnetii transmission is primarily ticks.', 'Ticks are the vector for coxiella burnetii transmission.', 'Ticks are the common vector for Coxiella burnetii', 'Yes, Coxiella burnetii is transmitted by ticks.', 'Ticks are the vectors for transmitting Coxiella burnetii.', 'Ticks, including species like Hyalomma lusitanicum, I. ricinus, and Ornithodoros moubata, act as vectors for the transmission of Coxiella burnetii.', 'The vector for Coxiella burnetii transmission is ticks, specifically through tick feces and saliva.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26186513",
"http://www.ncbi.nlm.nih.gov/pubmed/37387368",
"http://www.ncbi.nlm.nih.gov/pubmed/32141019",
"http://www.ncbi.nlm.nih.gov/pubmed/26458781",
"http://www.ncbi.nlm.nih.gov/pubmed/32059686",
"http://www.ncbi.nlm.nih.gov/pubmed/33406079",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37387368",
"endSection": "abstract",
"offsetInBeginSection": 334,
"offsetInEndSection": 484,
"text": "transmitted by ticks include bacteria of the genus Borrelia and the species Francisella tularensis, Anaplasma ph... | 13 | BioASQ-training13b | null | null | 65f039fdc4010b4d78000002 |
factoid | What is an Albatross plot used for? | ['visualization of diversely reported studies'] | ['An albatross plot is a novel graphical tool for presenting results of diversely reported studies in a systematic review.', 'An Albatross plot is a graphical representation of the distribution of the number of patients with a given outcome in a clinical trial. It is used to visualize the distribution of outcomes in a trial and to identify potential issues with the trial design or conduct.', 'An Albatross plot is a graphical tool used in systematic reviews to present the results of diversely reported studies. It helps to visualize and compare the findings of different studies, making it easier to identify patterns and trends in the data.', 'The albatross plot is a novel graphical tool for presenting results of diversely reported studies in a systematic review', 'The albatross plot is a novel graphical tool for presenting results of diversely reported studies in a systematic review.', 'An Albatross plot is used to present the results of diversely reported studies in a systematic review in a graphical format.', 'The Albatross plot is used for presenting the results of studies that are reported in diverse ways within a systematic review.', 'An Albatross plot is used for presenting results of diversely reported studies in a systematic review.', 'An Albatross plot is a novel graphical tool used for presenting the results of diversely reported studies in a systematic review. It helps to visually display the effect sizes and confidence intervals of individual studies, allowing for a comprehensive overview of the data and facilitating the interpretation of the overall findings.', 'The Albatross plot is used for presenting results of diversely reported studies in a systematic review.', 'Albatross plot is a graphical tool used in systematic reviews to present the results of studies that report the effect size or estimate for an outcome in diverse ways. It allows visual comparison of studies by displaying the effect size and confidence interval in a single plot.', 'An Albatross plot is used to visually present the results of studies that are reported in diverse ways within a systematic review, showing the estimated direction of effects and helping interpret P values based on study sample sizes.', 'An Albatross plot is a graphical tool utilized in systematic reviews. Its primary function is to present the results of studies that have been reported in diverse ways, providing a visual representation that aids in the interpretation and comparison of these results.', 'An Albatross plot is used for meta-analyses to combine the results of multiple studies of a common question. It allows an approximate examination of underlying effect sizes and the potential to identify sources of heterogeneity across studies.', 'An Albatross plot is used for presenting the results of studies that are reported in diverse ways in a systematic review. It provides a graphical tool for visualizing and interpreting these results.', 'An Albatross plot is a novel graphical tool for presenting results of diversely reported studies in a systematic review.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28453179",
"http://www.ncbi.nlm.nih.gov/pubmed/34035181",
"http://www.ncbi.nlm.nih.gov/pubmed/32423407"
] | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28453179",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "The albatross plot: A novel graphical tool for presenting results of diversely reported studies in a systematic review."... | 13 | BioASQ-training13b | null | null | 65f37997c4010b4d7800000b |
factoid | What disorder is considered off label use for domperidone? | ['inducing lactation', 'Gastroparesis'] | ['Domperidone is considered off-label use for inducing lactation in breastfeeding mothers.', 'Domperidone is used off-label for the purpose of inducing lactation.', 'Domperidone is commonly used off-label as a galactagogue to increase breast milk production.', 'Domperidone is a selective dopamine D2 receptor antagonist that was first developed as an antiemetic agent. The use of Domperidone in gastroparesis is off-label due to its peripheral effects. The main objective of this study is to assess quercetin antiemetic properties and domperidone as a positive control.', 'Domperidone is considered off-label for the treatment of functional dyspepsia.', 'Domperidone is used off-label to promote lactation in prolactin-deficient women.', 'Domperidone is a dopamine-2 antagonist used off-label to increase breast milk production.', 'Domperidone is commonly used off-label to induce lactation in women.', 'Domperidone is used off-label to induce lactation in prolactin-deficient women.', 'Domperidone is commonly used off-label to induce lactation in prolactin-deficient women.', 'Domperidone is considered off label use for gastroparesis.', 'Domperidone is considered off label use for lactation.', 'Domperidone is considered off-label for promoting lactation in prolactin-deficient women.', 'Inducing lactation, acute gastroenteritis treatment in pediatric patients, acute dystonia', 'Domperidone is used off label for the treatment of gastroparesis.', 'Domperidone is a medication most commonly used by pediatric gastroenterologists for treatment of symptoms associated with gastro-esophageal reflux disease, dyspepsia, and gastroparesis outside its authorized indication, i.e. off label use', 'Domperidone is a medication commonly used off-label for its potential to stimulate prolactin secretion and thus milk production.', 'Domperidone is commonly used off-label to stimulate milk production in mothers who have low milk supply. It is prescribed off-label in Canada and Australia to promote lactation in prolactin-deficient women.', 'Domperidone is considered an off-label treatment for functional dyspepsia.', 'Domperidone is considered off label use for lactation, prolactin-deficient women, and Lactation induction.', 'A major side effect of domperidone is prolactinemia, allowing it to be used off-label for the purpose of inducing lactation.', 'Domperidone is considered off-label for the disorder of lactation, specifically to induce lactation by acting as a dopamine-2 antagonist.', ' Domperidone is considered off-label use for prolactin-deficient women to increase breast milk production.', 'Domperidone is an antiemetic that is commonly used off-label to induce lactation in prolactin-deficient women.', 'Domperidone is an antiemetic that is commonly used as an off-label prescription to induce lactation.', 'Domperidone is commonly used as an off-label prescription to induce lactation and increase breast milk production in women with prolactin deficiency.', 'Domperidone is used off label for treating symptoms related to gastro-esophageal reflux disease, dyspepsia, and gastroparesis.', 'Domperidone is often used off-label for the treatment of lactation deficiency. It helps to increase the production of breast milk.', 'Domperidone is considered an off-label treatment for promoting lactation in prolactin-deficient women.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37352416",
"http://www.ncbi.nlm.nih.gov/pubmed/25306766",
"http://www.ncbi.nlm.nih.gov/pubmed/35793516",
"http://www.ncbi.nlm.nih.gov/pubmed/25475074",
"http://www.ncbi.nlm.nih.gov/pubmed/25825854",
"http://www.ncbi.nlm.nih.gov/pubmed/24600732",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35793516",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 113,
"text": "Domperidone is an antiemetic that is commonly used as an off-label prescription to induce lactation. "
},
{
... | 13 | BioASQ-training13b | null | null | 65f493cac4010b4d78000012 |
factoid | What is the most common surgical treatment for hydrocephalus? | ['Ventriculoperitoneal shunt'] | ["The most common surgical treatment for hydrocephalus is Ventriculoperitoneal (VP) shunting, which involves the placement of a shunt system to divert excess cerebrospinal fluid from the brain's ventricles to the abdominal cavity, where it can be absorbed by the body.", 'The most common surgical treatment for hydrocephalus is the placement of a ventriculoperitoneal shunt.', 'Ventriculoperitoneal (VP) shunt surgery is the most widely used neurosurgical procedure for the management of hydrocephalus.', 'Ventriculoperitoneal (VP) shunting is the most common neurosurgical treatment for hydrocephalus.', 'The most common surgical treatment for hydrocephalus is ventriculoperitoneal (VP) shunt placement. This procedure involves the insertion of a catheter into the ventricles of the brain to divert excess cerebrospinal fluid (CSF) into the peritoneal cavity, where it can be absorbed by the body.', 'The most common surgical treatment for hydrocephalus is ventriculoperitoneal shunt (VPS) insertion.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22650109",
"http://www.ncbi.nlm.nih.gov/pubmed/35609726",
"http://www.ncbi.nlm.nih.gov/pubmed/25569424",
"http://www.ncbi.nlm.nih.gov/pubmed/17946960",
"http://www.ncbi.nlm.nih.gov/pubmed/30459864",
"http://www.ncbi.nlm.nih.gov/pubmed/21961546",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34152450",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 360,
"text": "Gravitation-assisted shunt valves are designed to prevent hydrostatic over-drainage frequently observed in the l... | 13 | BioASQ-training13b | null | null | 65f85ec7c4010b4d78000052 |
factoid | Gantenerumab was developed for treatment of which disease? | ["Alzheimer's disease"] | ["Gantenerumab was developed for Alzheimer's disease."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/24445401",
"http://www.ncbi.nlm.nih.gov/pubmed/32787971",
"http://www.ncbi.nlm.nih.gov/pubmed/26433971",
"http://www.ncbi.nlm.nih.gov/pubmed/29221491",
"http://www.ncbi.nlm.nih.gov/pubmed/36457865",
"http://www.ncbi.nlm.nih.gov/pubmed/34155411",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35841240",
"endSection": "abstract",
"offsetInBeginSection": 259,
"offsetInEndSection": 442,
"text": "Other anti-amyloid antibodies are under investigation in phase III (donanemab, lecanemab, gantenerumab) and have... | 13 | BioASQ-training13b | null | null | 65cfa37c1930410b1300000d |
factoid | What is the administration route of zavegepant? | ['intranasally', 'nasal spray'] | ['Zavegepant is administered intranasally and used for migraine attacks.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37227596",
"http://www.ncbi.nlm.nih.gov/pubmed/37345774",
"http://www.ncbi.nlm.nih.gov/pubmed/33096162",
"http://www.ncbi.nlm.nih.gov/pubmed/36804093",
"http://www.ncbi.nlm.nih.gov/pubmed/37904462",
"http://www.ncbi.nlm.nih.gov/pubmed/37363553",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37345774",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Zavegepant (Zavzpret), a nasal spray, is approved to treat adults with acute migraine with or without aura."
},
... | 13 | BioASQ-training13b | null | null | 65d1357c1930410b13000039 |
factoid | What is the first line treatment for severe Plasmodium falciparum malaria? | ['Artesunate', 'intravenous artesunate', 'IV artesunate', 'parenteral artesunate'] | ['Intravenous artesunate', 'parenteral artesunate (ARS)', 'Parenteral artesunate is the first-line treatment for severe Plasmodium falciparum malaria.', 'Parenteral artesunate (ARS) is the first-line treatment for severe falciparum malaria.', 'Intravenous artesunate is the first-line treatment for severe falciparum malaria.', 'Intravenous artesunate is the first-line treatment for severe Plasmodium falciparum malaria. If artesunate is not available, intravenous quinine should be started immediately as an alternative treatment.', 'The first-line treatment for severe Plasmodium falciparum malaria is intravenous artesunate.', 'Intravenous artesunate is the first line treatment for severe Plasmodium falciparum malaria.', '- For severe Plasmodium falciparum malaria, intravenous artesunate is the recommended first-line treatment. Intravenous artesunate is administered for 24 hours after clinical improvement is observed, followed by a full course of artemisinin-based combination therapy (ACT).', 'Parenteral artesunate (ARS) is the first-line treatment for severe Plasmodium falciparum malaria.', 'Yes, artesunate is the first-line treatment for severe malaria.', 'Parenteral artesunate is the first-line treatment for severe falciparum malaria.', 'Intravenous artesunate is the first-line treatment for severe Plasmodium falciparum malaria.', 'The first-line treatment for severe Plasmodium falciparum malaria is parenteral artesunate (ARS), which can be administered intravenously or intramuscularly.', 'The first-line treatment for severe Plasmodium falciparum malaria is parenteral artesunate (ARS). This is the global standard of care for severe malaria.', 'The first-line treatment for severe Plasmodium falciparum malaria is parenteral artesunate (ARS). This is also known as intravenous artesunate and is recognized as the global standard of care for severe malaria.', 'Intravenous artesunate is the first-line treatment and global standard of care for severe falciparum malaria.', 'Injectable artesunate is the first line treatment for severe Plasmodium falciparum malaria.', 'The first-line treatment for severe Plasmodium falciparum malaria is intravenous artesunate. WHO recommends artesunate for the first 24 hours, followed by a combination of artemisinin derivatives and oral lumefantrine, for a total of 3 days.', 'The first-line treatment for severe Plasmodium falciparum malaria is parenteral artesunate (ARS).', 'First line treatment in severe Plasmodium falciparum malaria is artesunate.', 'The first-line treatment for severe Plasmodium falciparum malaria is injectable artesunate.', 'First-line treatment of severe P. falciparum malaria is based on IV artesunate.', 'The first-line treatment for severe Plasmodium falciparum malaria is parenteral or intravenous artesunate.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/30885541",
"http://www.ncbi.nlm.nih.gov/pubmed/36056897",
"http://www.ncbi.nlm.nih.gov/pubmed/34561157",
"http://www.ncbi.nlm.nih.gov/pubmed/22453057",
"http://www.ncbi.nlm.nih.gov/pubmed/36126008",
"http://www.ncbi.nlm.nih.gov/pubmed/23350023",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36056897",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "Intravenous artesunate has been the global standard of care for severe malaria"
},
{
"beginSection": "abstr... | 13 | BioASQ-training13b | null | null | 65f82058c4010b4d7800003d |
factoid | What is the use of lebrikizumab? | ['atopic dermatitis'] | ['Lebrikizumab scan be used for moderate-to-severe atopic dermatitis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37266844",
"http://www.ncbi.nlm.nih.gov/pubmed/36630140",
"http://www.ncbi.nlm.nih.gov/pubmed/36948491",
"http://www.ncbi.nlm.nih.gov/pubmed/36994947",
"http://www.ncbi.nlm.nih.gov/pubmed/37401345"
] | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36630140",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Efficacy and Safety of Lebrikizumab in Combination With Topical Corticosteroids in Adolescents and Adults With Moderate-... | 13 | BioASQ-training13b | null | null | 65d36e761930410b13000044 |
factoid | Coffee Bean Sign is characteristic to which disease? | ['volvulus', 'sigmoid volvulus'] | ['Coffee Bean Sign is characteristic to volvulus.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37761402",
"http://www.ncbi.nlm.nih.gov/pubmed/35773776",
"http://www.ncbi.nlm.nih.gov/pubmed/33088563",
"http://www.ncbi.nlm.nih.gov/pubmed/36168370",
"http://www.ncbi.nlm.nih.gov/pubmed/18322966",
"http://www.ncbi.nlm.nih.gov/pubmed/36779459",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35773776",
"endSection": "abstract",
"offsetInBeginSection": 1020,
"offsetInEndSection": 1669,
"text": ". In addition, X-ray signs including disproportionate sigmoid dilatation, distended inverted 'U' in sigmoid, c... | 13 | BioASQ-training13b | null | null | 65d144b81930410b13000041 |
factoid | What process does tRNA nucleotidyl transferase 1 (TRNT1) catalyze? | ["Addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs)"] | ["tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs).", 'The tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs, which is necessary for aminoacylation.', "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of CCA nucleotides to the 3' end of tRNA molecules during tRNA maturation.", "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), which is essential for translation and functions in both the cytoplasm and mitochondria.", "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), a crucial process for translation.", "The TRNT1 enzyme catalyzes the addition of the trinucleotide CCA to the 3' end of tRNAs.", 'TRNT1 gene encodes a CCA-adding tRNA nucleotidyl transferase enzyme.', "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine-cytosine-adenine (CCA) sequence to the 3' end of transfer RNAs (tRNAs). This CCA addition is essential for tRNA function in protein translation.", "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), which is essential for translation", 'tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs, which is necessary for aminoacylation.', "3'-tRNA nucleotidyl transferase (TRNT1) is an enzyme that catalyzes the terminal nucleotidyl transfer of CCA sequence to the 3'-end of tRNA, which is essential for tRNA function in protein translation.", "TRNT1 catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), which is essential for translation.", "tRNA Nucleotidyl Transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), a process essential for translation.", "TRNT1 (tRNA nucleotidyl transferase) catalyzes the addition of the CCA to the 3' end of tRNAs.", "tRNA Nucleotidyl Transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs). This process is essential for translation.", "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), which is essential for translation.", "Addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs) is essential for translation and is catalyzed by the enzyme TRNT1 (tRNA nucleotidyl transferase),", "TRNT1 catalyzes the addition of a CCA nucleotide to the 3' end of tRNA molecules", 'tRNA nucleotidyl transferase 1 (TRNT1) is an essential enzyme catalyzing the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs, which is necessary for aminoacylation.', 'TRNT1 catalyzes the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs.', "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the invariant CCA-terminus to the tRNA 3'-end, which is a central step in tRNA maturation and is necessary for aminoacylation.", 'TRNT1 is an enzyme that catalyzes the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs.', 'The tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs.', "The tRNA Nucleotidyl Transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs). This process is essential for translation and occurs in both the cytoplasm and mitochondria"] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36646204",
"http://www.ncbi.nlm.nih.gov/pubmed/15265870",
"http://www.ncbi.nlm.nih.gov/pubmed/29884622",
"http://www.ncbi.nlm.nih.gov/pubmed/26172425",
"http://www.ncbi.nlm.nih.gov/pubmed/884105",
"http://www.ncbi.nlm.nih.gov/pubmed/32181284",
"http://www.ncbi.nlm.nih... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36121781",
"endSection": "abstract",
"offsetInBeginSection": 162,
"offsetInEndSection": 231,
"text": "TRNT1 gene encodes a CCA-adding tRNA nucleotidyl transferase enzyme. "
},
{
"beginSection": "abstract",
... | 13 | BioASQ-training13b | null | null | 662cfc88187cba990d000008 |
factoid | What is the prevalence of intellectual developmental disorders in Becker Muscular Dystrophy? | ['8%'] | ['The global prevalence of intellectual developmental disorder (IDD) is 8% in Becker muscular dystrophy.', 'The global prevalence of intellectual developmental disorder (IDD) in Becker muscular dystrophy (BMD) is 8%.', 'The prevalence of intellectual developmental disorders in Becker Muscular Dystrophy is 8%.', 'The global prevalence of intellectual developmental disorder (IDD) was 8% in Becker muscular dystrophy.', 'The global prevalence of intellectual developmental disorder (IDD) in Becker muscular dystrophy is 8%.', 'The prevalence of intellectual developmental disorders in Becker Muscular Dystrophy is 8%', 'The prevalence of intellectual developmental disorders in Becker Muscular Dystrophy is estimated to be 8.3%.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36440509"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36440509",
"endSection": "abstract",
"offsetInBeginSection": 1369,
"offsetInEndSection": 1471,
"text": "The global prevalence of intellectual developmental disorder (IDD) was 8% in Becker muscular dystrophy"
},
... | 13 | BioASQ-training13b | null | null | 66300d3e187cba990d00001b |
factoid | Mutation of which gene was implicated in Disabling pansclerotic morphea? | ['STAT4'] | ['Gain-of-function variants in STAT4 was implicated in Disabling pansclerotic morphea.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37256972"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37256972",
"endSection": "abstract",
"offsetInBeginSection": 1531,
"offsetInEndSection": 1622,
"text": "CONCLUSIONS: Gain-of-function variants in STAT4 caused DPM in the families that we studied."
},
{
"beg... | 13 | BioASQ-training13b | null | null | 65cfdf1c1930410b13000028 |
factoid | Oxysterol is produced by the oxidation of what waxy, fat-like substance made in the liver? | ['Cholesterol'] | ['Oxysterols are produced by the oxidation of cholesterol.', 'Oxysterols are derived from either enzymatic or non-enzymatic oxidation of cholesterol.', 'Oxysterol is produced by the oxidation of cholesterol, a waxy, fat-like substance that is synthesized in the liver.', "Oxysterols are produced by the oxidation of cholesterol, a waxy, fat-like substance that is primarily synthesized in the liver, the body's main metabolic organ.", 'Oxysterols are produced by the oxidation of cholesterols in the liver.', '7-Ketocholesterol is an oxysterol produced by the oxidation of cholesterol, a waxy, fat-like substance made in the liver.', 'Oxysterol is produced by the oxidation of cholesteryl esters in the liver.', 'Cholesterol is a waxy, fat-like substance made in the liver that is necessary for many bodily functions, and oxysterols are produced by the oxidation of cholesterol.', 'Oxysterols are produced by the oxidation of cholesterol, a waxy, fat-like substance that is made in the liver', 'Oxysterol is produced by the oxidation of cholesterol', 'Oxysterol is produced by the oxidation of cholesterol, a waxy, fat-like substance made in the liver', 'Oxysterols derive from either enzymatic or non-enzymatic oxidation of cholesterol.', 'Oxysterol is produced by the oxidation of cholesterol.', '7-alpha hydroxycholesterol, also known as 7-OHC, is an oxysterol produced by the oxidation of cholesterol.', 'Oxysterols are produced by the oxidation of cholesterol, which is a waxy, fat-like substance made in the liver.', 'Oxysterol is produced by the oxidation of cholesterol, a waxy, fat-like substance made in the liver.', 'Oxysterols are produced by the oxidation of cholesterol, a waxy, fat-like substance made in the liver.', 'Oxysterol is produced by the oxidation of the waxy, fat-like substance made in the liver, cholesterol.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22026270",
"http://www.ncbi.nlm.nih.gov/pubmed/24333430",
"http://www.ncbi.nlm.nih.gov/pubmed/11111082",
"http://www.ncbi.nlm.nih.gov/pubmed/38036890",
"http://www.ncbi.nlm.nih.gov/pubmed/19248802",
"http://www.ncbi.nlm.nih.gov/pubmed/25255963",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38036887",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Oxysterols derive from either enzymatic or non-enzymatic oxidation of cholesterol. "
},
{
"beginSection": "... | 13 | BioASQ-training13b | null | null | 662a4b08b9f8b89d7e00000b |
factoid | Which chromosome is most commonly affected by loss of heterozygosity in glioblastoma? | ['Chromosome 10', '10'] | ['Glioblastomas develop de novo (primary glioblastomas) or through progression from low-grade or anaplastic astrocytoma (secondary glioblastomas). There is increasing evidence that these glioblastoma subtypes develop through different genetic pathways. Loss of heterozygosity (LOH) on chromosome 10 is the most frequent genetic alteration in glioblastomas. In particular, LOH on 10q is a major factor in the evolution of glioblastoma multiform as the common phenotypic endpoint of both genetic pathways, whereas LOH on 10p is largely restricted to the primary glioblastoma.', 'The most common genetic alteration in glioblastomas is loss of heterozygosity (LOH) on chromosome 10. This chromosomal loss is a significant factor in the development of glioblastoma multiform, which can occur through two different genetic pathways: de novo (primary glioblastomas) or progression from low-grade or anaplastic astrocytoma (secondary glioblastomas). LOH on 10q is a major factor in the evolution of glioblastoma multiform for both genetic pathways, while LOH on 10p is predominantly restricted to the primary (de novo) glioblastoma. In summary, chromosome 10 is the chromosome most commonly affected by LOH in glioblastoma.', 'The most frequent genetic alteration in glioblastomas, a type of brain tumor, is the loss of heterozygosity (LOH) on chromosome 10. This occurs specifically on the long arm of chromosome 10, denoted as LOH 10q. This genetic change is common to both primary and secondary glioblastomas, suggesting it plays a significant role in the development and progression of these tumors. While LOH on 10p also occurs, it is mostly restricted to primary (de novo) glioblastomas. Therefore, chromosome 10, particularly 10q, is the most commonly affected chromosome by LOH in glioblastoma.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/17691218",
"http://www.ncbi.nlm.nih.gov/pubmed/10604735",
"http://www.ncbi.nlm.nih.gov/pubmed/28960585",
"http://www.ncbi.nlm.nih.gov/pubmed/8641967",
"http://www.ncbi.nlm.nih.gov/pubmed/34970477",
"http://www.ncbi.nlm.nih.gov/pubmed/9591629",
"http://www.ncbi.nlm.nih... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10653004",
"endSection": "abstract",
"offsetInBeginSection": 439,
"offsetInEndSection": 551,
"text": "Loss of heterozygosity (LOH) on chromosome 10 (LOH#10) is the most frequent genetic alteration in glioblastomas;... | 13 | BioASQ-training13b | null | null | 6630154c187cba990d000021 |
factoid | Which genetic alteration is most commonly associated with the classical subtype of glioblastoma? | ['Epidermal growth factor receptor (EGFR) amplification', 'EGFR amplification', 'EGFR gene amplification', 'Amplification of the epidermal growth factor receptor (EGFR)', 'EGFR overexpression', 'high EGFR expression'] | ['The classical subtype of glioblastoma is most commonly associated with epidermal growth factor receptor (EGFR) gene amplification, occurring in 40-60% of cases. Despite EGFR overexpression contributing to the aggressive nature of GBM and numerous clinical trials for targeted therapies, no significant benefits have been reported due to resistance factors such as tumor heterogeneity, alternative pathways, and blood-brain barrier. Further understanding of these mechanisms is crucial for effective treatment strategies.', 'Despite all of the progress in understanding its molecular biology and pathogenesis, glioblastoma (GBM) is one of the most aggressive types of cancer, and without an efficient treatment modality at the moment, it remains largely incurable. Nowadays, it is known that epidermal growth factor receptor (EGFR) amplification is one of the most commonly associated genetic alterations of the classical subtype of glioblastoma. However, targeted therapies against this type of receptor have not yet shown a clear clinical benefit.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37446288",
"http://www.ncbi.nlm.nih.gov/pubmed/22539962",
"http://www.ncbi.nlm.nih.gov/pubmed/24410805",
"http://www.ncbi.nlm.nih.gov/pubmed/26757882",
"http://www.ncbi.nlm.nih.gov/pubmed/34608482",
"http://www.ncbi.nlm.nih.gov/pubmed/33053208",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37446288",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 598,
"text": "Despite all of the progress in understanding its molecular biology and pathogenesis, glioblastoma (GBM) is one of ... | 13 | BioASQ-training13b | null | null | 663016bb187cba990d000023 |
factoid | What is PUL-2 in Duchenne Muscular Dystrophy? | ['Performance of Upper Limb', 'assessement measure of upper limb function'] | ['PUL 2.0 is the performance of upper limb 2.0 (PUL) and is widely used to assess upper limb function in DMD patients.', 'PUL-2, or Performance of the Upper Limb 2.0, is a measure used to assess upper limb function in patients with Duchenne Muscular Dystrophy.', 'The Performance of Upper Limb version 2.0 (PUL 2.0) is a widely used tool to assess upper limb function in Duchenne Muscular Dystrophy patients.', 'PUL 2.0 or Performance of Upper Limb 2.0 is a tool used to assess the function of the upper limbs in patients with Duchenne Muscular Dystrophy (DMD).', 'PUL-2, or Performance of Upper Limb 2.0, is a standardized assessment tool used to evaluate upper limb function in Duchenne Muscular Dystrophy (DMD) patients', 'PUL (Performance of Upper Limb) 2.0 is a widely used assessment tool to evaluate upper limb function in patients with Duchenne Muscular Dystrophy (DMD).', 'The performance of upper limb 2.0 in Duchenne Muscular Dystrophy is an assessment tool used to evaluate upper limb function in DMD patients.', 'The performance of upper limb 2.0 (PUL) is a widely used assessment tool to evaluate upper limb function in Duchenne Muscular Dystrophy (DMD) patients.', 'The performance of upper limb 2.0 (PUL) is widely used to assess upper limb function in DMD patients', 'The performance of upper limb 2.0 (PUL) is widely used to assess upper limb function in Duchenne Muscular Dystrophy.', 'PUL-2, or Performance of Upper Limb 2.0, is a tool used to assess upper limb function in patients with Duchenne Muscular Dystrophy (DMD).', 'The Performance of Upper Limb 2.0 (PUL-2) in Duchenne Muscular Dystrophy is a widely used assessment tool for evaluating upper limb function in patients with this condition.', 'PUL 2.0 (Performance of Upper Limb 2.0) is a functional assessment tool used to evaluate upper limb function in patients with Duchenne muscular dystrophy (DMD). It measures the ability to perform various upper limb tasks and helps track disease progression and treatment effects in DMD.', 'PUL-2 is a clinical scale for assessing the performance of the upper limb in patients with Duchenne muscular dystrophy.', 'The performance of upper limb 2.0 (PUL) is widely used to assess upper limb function in DMD patients.', 'PUL-2 is a component of the Performance of Upper Limb 2.0 (PUL) assessment tool, which is used to evaluate upper limb function in patients with Duchenne Muscular Dystrophy (DMD).', 'The Performance of Upper Limb version 2.0 (PUL 2.0) is increasingly used in Duchenne Muscular Dystrophy (DMD) to study longitudinal functional changes of motor upper limb function in ambulant and non-ambulant patients.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37066919"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37066919",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 113,
"text": "The performance of upper limb 2.0 (PUL) is widely used to assess upper limb function in DMD patients."
}
] | 13 | BioASQ-training13b | null | null | 66302487187cba990d000031 |
factoid | What is the average median survival for advanced colorectal cancer patients? | ['32.4 months', '32 months', '24-30 months'] | ['In summary, based on the provided data, the average median overall survival (OS) of advanced colorectal cancer patients has improved over time from approximately 22.6 months between 2004 and 2012 to around 32.4 months for those diagnosed between 2016 and 2019. The weighted average median survival for the entire period is about 28.0 months.', 'According to the abstracts provided, the average median survival for advanced colorectal cancer patients varies depending on the specific study and population. However, based on the information presented, it can be concluded that: * The median overall survival for metastatic colorectal cancer is nearly 2 years (Abstract 1). * Median survival in advanced colorectal cancer patients treated with 5-fluorouracil (5FU) and leucovorin (LV) is between 12 and 18 months, with a specific study reporting a median survival of 18 months (Abstract 3). * The median survival for advanced CRC reported in clinical trials now approaches 2 years (Abstract 4). * In untreated advanced colorectal cancer patients, the median survival was found to be 24 months (range 16-42) (Abstract 5). , Overall, the average median survival for advanced colorectal cancer patients appears to be around 18-24 months.', 'The average median survival for advanced colorectal cancer patients is 20 months.The addition of ramicurumab to second line therapy significantly improved median overall survival.KRAS gene mutation in colorectal cancer patients is closely associated with poor prognosis.Obesity is a risk factor for poor overall survival in patients with colorectal cancer.EGFR, primary tumor site, and multiple metastases of tumor are independent risk factors for poor overall survival in patients with colorectal cancer.Fluorouracil has been the mainstay of chemotherapy for advanced colorectal cancer for over 40 years and is effective in prolonging time to disease progression and survival.', 'Median OS was roughly stable for patients diagnosed between 2004 and 2012 (22.6 months) but since has steadily improved for those diagnosed in 2013 to 2015 (28.8 months), and 2016 to 2019 (32.4 months.', 'The average median survival for advanced colorectal cancer patients is 25 months.', 'The average median survival for advanced colorectal cancer patients has been roughly stable for those diagnosed between 2004 and 2012 at 22.6 months, but has shown a steady improvement for those diagnosed in 2013 to 2015 (28.8 months) and 2016 to 2019 (32.4 months).', 'Median OS was roughly stable for patients diagnosed between 2004 and 2012 (22.6 months) but since has steadily improved for those diagnosed in 2013 to 2015 (28.8 months), and 2016 to 2019 (32.4 months)', '32.4 months\n\nContext: The median OS was 22.6 months for patients diagnosed between 2004 and 2012, 28.8 months for those diagnosed in 2013 to 2015, and 32.4 months for those diagnosed in 2016 to 2019.\nQuestion: What is the average median survival for advanced colorectal cancer patients?\nAnswer: 32.4 months\n\nContext: The median OS was 22.6 months for patients diagnosed between 2004 and 2012, 28.8 months for those diagnosed in 2013 to 2015, and 32.4 months for those diagnosed in 2016 to 2019.\nQuestion: What is the average median survival for advanced colorectal cancer patients?\nAnswer: 32.4 months\n\nContext: The median OS was 22.6 months for patients diagnosed between 2004 and 2012, 28.8 months for those diagnosed in 2013 to 2015, and 32.4 months for those diagnosed in 2016 to 2019.\nQuestion: What is the average median survival for advanced colorectal cancer patients?\nAnswer: 32.4 months\n\nContext:', 'The average median survival for advanced colorectal cancer patients has steadily improved over time, with the median OS being 22.6 months for those diagnosed between 2004 and 2012, 28.8 months for those diagnosed in 2013 to 2015, and 32.4 months for those diagnosed in 2016 to 2019.', 'The average median survival for advanced colorectal cancer patients is approximately 20-24 months based on various studies; however, the median overall survival has increased over time due to advancements in treatment strategies.', 'The average median survival for advanced colorectal cancer patients has improved over time. For patients diagnosed between 2004 and 2012, the median OS was 22.6 months, while for those diagnosed in 2013 to 2015, it was 28.8 months, and for those diagnosed in 2016 to 2019, it was 32.4 months.', 'The average median survival time for advanced colorectal cancer patients is approximately 15 months. This is based on the data from several studies that report median survival times ranging from 6 to 25 months. It is important to note that the survival time can vary depending on the stage of the disease, the treatment regimen, and other patient-specific factors.', 'Based on the provided information, the median survival time for patients with advanced or metastatic colorectal cancer ranges from approximately 6 to 25 months, depending on factors such as extent of metastases and treatment received.\n\nWithout treatment, median survival is around 7.5 to 11 months. Systemic chemotherapy modestly improves median survival to about 12 months. More aggressive treatments like regional chemotherapy or combined chemotherapy regimens (e.g. FOLFOX, FOLFIRI) can extend median survival further to 15-17 months or even up to 23-25 months in some cases.\n\nHowever, even with treatment, 5-year survival rates remain low, ranging from under 5% to 31%. Advanced colorectal cancer is rarely curable, although treatments can prolong survival. Median survival is highly variable based on individual patient and cancer characteristics.', "The average median survival for advanced colorectal cancer patients, based on the abstracts provided, appears to be around 7 months. This estimate comes from a review of the natural history of disseminated colorectal cancer, which states that the overall median survival rate of patients with hepatic metastases from colorectal primary cancer is approximately 7 months. However, it's important to note that many patients survive for three years and some even live for more than ten years without any specific treatment. This variability in survival times underscores the complex nature of colorectal cancer and the importance of personalized medical approaches.", 'The median overall survival (OS) for patients diagnosed with advanced colorectal cancer has been improving over the years. For those diagnosed between 2004 and 2012, it was roughly 22.6 months. It improved to 28.8 months for those diagnosed between 2013 and 2015, and further improved to 32.4 months for those diagnosed between 2016 and 2019.', 'The average median survival for advanced colorectal cancer patients is 32.4 months.', "22.6 months for patients diagnosed between 2004 and 2012, 28.8 months for those diagnosed in 2013 to 2015, and 32.4 months for those diagnosed in 2016 to 2019. \n\nPlease go ahead and ask your question. I'll do my best to provide a concise answer. \n\n(Note: Please keep your question related to the context provided.)", "The average median survival for advanced colorectal cancer patients is not explicitly stated in the provided Wikipedia articles. However, the articles mention that the five-year survival rate in the United States was around 65% in 2014, and the individual likelihood of survival depends on factors such as the stage of the cancer, the ability to remove the cancer surgically, and the person's overall health. The articles also discuss various treatment options for colorectal cancer, including surgery, radiation therapy, chemotherapy, and targeted therapy, as well as the importance of early detection and prevention through lifestyle changes and regular screenings.\n\nBased on the provided articles, the median survival time for patients with inoperable liver metastases from colorectal cancer is 7.4 to 11 months. Systemic chemotherapy produces a modest improvement to 12 months, while regional chemotherapy produces a further improvement to 15 to 17 months. The median survival time after diagnosis of metastases is almost comparable with 17 months. The median survival time was 6 months in the entire cohort, 16 months, 7.5 months, 8.5 months for all patients, 11 months for patients with solitary hepatic tumour, and 7.5 months for those with multiple tumours. Combined with regimens such as FOLFOX or FOLFIRI, median survival rates have been increased to an average of 23 months. The 1Y-PFS was 28.5% (median survival time (MST): 7.4 months), 1Y-OS was 76.6% (MST not reached), 3Y-PFS was 5.5% (MST: 7.4 months), and 3Y-OS was 26.4% (MST: 25.2 months).", 'The average median overall survival (OS) of advanced colorectal cancer patients has improved over time: 22.6 months for diagnoses between 2004 and 2012, 28.8 months for those diagnosed between 2013 and 2015, and 32.4 months for those diagnosed between 2016 and 2019. The average median survival across these periods is approximately 28.0 months.', 'The average median survival for advanced colorectal cancer patients is 32.4 months, 28.8 months, and 22.6 months for the years 2016 to 2019, 2013 to 2015, and 2004 to 2012 respectively.', 'The median overall survival (OS) for advanced colorectal cancer patients has improved over time:\n\n- For those diagnosed between 2004 and 2012, median OS was roughly stable at 22.6 months\n- For those diagnosed from 2013 to 2015, median OS improved to 28.8 months \n- Most recently, for patients diagnosed between 2016 to 2019, the median OS further increased to 32.4 months\n\nIn summary, the average median survival for advanced colorectal cancer patients diagnosed in recent years is around 32 months, representing a substantial improvement compared to earlier time periods.', 'The average median survival for advanced colorectal cancer (CRC) patients cannot be precisely determined from the provided text, as it presents data on overall survival (OS) improvements over time at a single institution, the University of Texas M.D. Anderson Cancer Center (UTMDACC). However, some key points can help approximate an answer: , 1. Median OS for de novo metastatic CRC patients at UTMDACC was 22.6 months for those diagnosed between 2004 and 2012., 2. For patients diagnosed from 2013 to 2015, the median OS improved to 28.8 months, and further increased to 32.4 months for those diagnosed from 2016 to 2019. , Considering these figures, a rough estimate of the average median survival for advanced CRC patients may fall between 22.6 and 32.4 months, with an understanding', 'The average median survival for advanced colorectal cancer patients has been improving over the years. It was roughly stable at 22.6 months for patients diagnosed between 2004 and 2012, improved to 28.8 months for those diagnosed in 2013 to 2015, and further improved to 32.4 months for those diagnosed in 2016 to 2019.', 'The average median survival for advanced colorectal cancer patients is between 12-20 months, however, this can vary based on many factors such as patient demographics, disease presentation, treatment response, and comorbidities.', 'The average median survival for advanced colorectal cancer patients has been improving over the years. For patients diagnosed between 2004 and 2012, the median overall survival (OS) was about 22.6 months. This improved to 28.8 months for those diagnosed between 2013 and 2015, and further increased to 32.4 months for those diagnosed between 2016 and 2019', 'The median time to worsening of the ECOG performance-status score from 0 or 1 to 2 or more was 9.3 months in the combination group and 6.3 months in the FTD-TPI group (hazard ratio, 0.54; 95% CI, 0.43 to 0.67).', 'The average median survival for patients with advanced colorectal cancer has slightly improved over the years. For those diagnosed between 2004 and 2012, the median overall survival (OS) was 22.6 months. However, there has been a steady increase in survival for more recently diagnosed patients. Those diagnosed between 2013 and 2015 had a median OS of 28.8 months, while those diagnosed between 2016 and 2019 experienced a further improvement in survival, with a median OS of 32.4 months. Therefore, on average, the median survival for advanced colorectal cancer patients is around 27-32 months, based on the most recent data.', "The average median survival for advanced colorectal cancer patients is around 65% in the United States, according to 2014 data. However, survival rates can vary significantly and depend on various factors, including the stage of the cancer, the effectiveness of treatment, and the patient's overall health. Median survival time for patients with inoperable liver metastases from colorectal cancer is 7.4 to 17 months. When combined with regimens such as FOLFOX or FOLFIRI, median survival rates have been increased to an average of 23 months.", 'The average median survival for advanced colorectal cancer patients has been improving, with it being 22.6 months for those diagnosed between 2004 and 2012, 28.8 months for those diagnosed between 2013 and 2015, and 32.4 months for those diagnosed between 2016 and 2019.', 'The average median survival for advanced colorectal cancer patients is 25 months, with hepatic metastases showing a median survival of 7 months and current patients having an expected median survival of 20 months.', 'Advanced or metastatic colorectal cancer is a deadly disease with poor prognosis. Median survival for such patients is around 22-24 months, however, with novel therapeutic interventions, its been improved slightly.', 'Based on the provided information, the median overall survival for patients with advanced colorectal cancer has been improving in recent years:\n\nFor patients diagnosed between 2004 and 2012, median overall survival was around 22.6 months. \n\nFor those diagnosed from 2013 to 2015, median overall survival increased to 28.8 months.\n\nMost recently, for patients diagnosed between 2016 and 2019, the median overall survival further improved to 32.4 months.\n\nSo in summary, while advanced colorectal cancer remains difficult to cure, treatment advances have extended median survival from under 2 years to nearly 3 years over the past 15 years. However, individual prognosis still depends on factors like extent of disease, treatment options, and overall health.', 'The average median survival for advanced colorectal cancer patients has improved from 22.6 months between 2004 and 2012 to 28.8 months for those diagnosed in 2013 to 2015, and further improved to 32.4 months for those diagnosed in 2016 to 2019', 'The average median survival for advanced colorectal cancer patients has steadily improved over the years. For patients diagnosed between 2004 and 2012, the median overall survival (OS) was roughly stable at 22.6 months. However, for those diagnosed in 2013 to 2015, the median OS improved to 28.8 months, and for those diagnosed in 2016 to 2019, the median OS further improved to 32.4 months.', 'The average median survival for advanced colorectal cancer patients is around 65% in the United States, according to 2014 data. However, the median overall survival for patients diagnosed between 2004 and 2012 was 22.6 months, but it has steadily improved for those diagnosed in 2013 to 2015 (28.8 months) and 2016 to 2019 (32.4 months).', 'The average median survival for advanced colorectal cancer patients is 20 months. The addition of ramicurumab to second-line therapy significantly improved median overall survival. Immunotherapy has shown promise in GI malignancies, with the combination of pembrolizumab and chemotherapy extending median survival in patients with advanced colorectal cancer to 21 months. KRAS gene mutation is a poor prognostic factor in colorectal cancer patients, and advanced age and high TNM stage are independent risk factors for postoperative outcome in early-stage colorectal cancer patients. Class II and III obesity is associated with a modestly increased risk of disease recurrence and death in colorectal cancer patients. Fluorouracil has been the mainstay of chemotherapy for advanced colorectal cancer for over 40 years, and its use has been shown to prolong time to disease progression and survival in these patients.', 'Based on the information provided, the median survival time for patients with advanced colorectal cancer, specifically those with liver metastases, ranges from approximately 6 to 17 months without treatment or with systemic chemotherapy alone. Some key findings:\n\n- Without treatment, median survival is around 7.4 to 11 months\n- With systemic chemotherapy, median survival improves modestly to around 12 months \n- Regional chemotherapy can further improve median survival to 15-17 months\n- More recent combination regimens like FOLFOX or FOLFIRI have increased median survival to around 23 months on average\n\nSo in summary, median survival for advanced colorectal cancer with liver metastases is quite poor, typically under 1.5 years, but modern chemotherapy regimens have improved this to almost 2 years. The exact median survival depends on the specific treatment approach.', " In summary, advanced colorectal cancer patients have varied survival outcomes depending on the extent and location of the disease, the patient's age, overall health status, and the effectiveness of available treatment options. Improvements in early detection and prompt initiation of appropriate chemoradiation regimens can help improve patient outcomes and reduce the need for extensive surgery and associated morbidity. ", '30 months is the average median survival for advanced colorectal cancer patients, however it can vary based on several factors such as patient age, general health status, treatment response and presence of metastatic disease.', 'The average median survival is close to 15 months and in best-case scenario approximately 40 months.', 'According to the abstracts, the average median survival for advanced colorectal cancer patients varies from study to study. In one study, the median overall survival was reported to be nearly 2 years (20 months). Another study found a median survival of 18 months with a range of 12-18 months. A third study reported a median survival of 24 months in untreated advanced colorectal cancer patients. Overall, the median survival for advanced colorectal cancer patients appears to range from approximately 18-24 months, with some studies reporting longer or shorter median survivals depending on the specific patient population and treatment regimens used.', 'The median survival for advanced colorectal cancer patients is 12-18 months.', 'Based on the provided snippets, it appears that the question refers to the median overall survival (OS) of advanced colorectal cancer patients. The snippets suggest a steady improvement in median OS over time. , The median OS was roughly stable at 22.6 months for patients diagnosed between 2004 and 2012. However, for those diagnosed between 2013 and 2015, the median OS improved to 28.8 months, and further increased to 32.4 months for patients diagnosed between 2016 and 2019. , To calculate the average median survival, we can take a weighted average of these values based on the number of years in each period. Assuming equal weights, the average median OS would be approximately (22.6 + 28.8 + 32.4) / 3 = 28.0 months. , Therefore, the average median survival for advanced colorectal cancer patients is roughly 28.0 months.', 'The average median survival for advanced colorectal cancer patients is approximately 20-24 months, but has shown improvement over time due to advancements in treatment strategies. However, exact values can vary between studies and patient groups.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36781990",
"http://www.ncbi.nlm.nih.gov/pubmed/1588370",
"http://www.ncbi.nlm.nih.gov/pubmed/22763194",
"http://www.ncbi.nlm.nih.gov/pubmed/7008761",
"http://www.ncbi.nlm.nih.gov/pubmed/15547753",
"http://www.ncbi.nlm.nih.gov/pubmed/10826427",
"http://www.ncbi.nlm.nih... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36781990",
"endSection": "abstract",
"offsetInBeginSection": 513,
"offsetInEndSection": 713,
"text": "Median OS was roughly stable for patients diagnosed between 2004 and 2012 (22.6 months) but since has steadily i... | 13 | BioASQ-training13b | null | null | 66099907fdcbea915f000015 |
factoid | Where in the body would the globus pallidus be found? | ['brain', 'basal ganglia'] | ['The globus pallidus is a structure found in the brain.', 'The globus pallidus would be found in the brain.', 'The globus pallidus can be found in the basal ganglia, thalamus, and putamen.', 'The globus pallidus would be found in the basal ganglia.', 'The globus pallidus is a part of the basal ganglia, which is a group of nuclei located deep within the cerebral hemispheres of the brain.', 'The globus pallidus is found in the brain.', 'The globus pallidus is found in the brain. It is part of the basal ganglia, which is involved in the control of voluntary motor movements.', 'The globus pallidus is located in the brain.', 'The globus pallidus is a structure in the brain', 'The globus pallidus is located in the brain, specifically in regions such as the substantia nigra and nucleus accumbens.', 'The globus pallidus is found in the basal ganglia.', 'Globus pallidus is one of the components of the basal ganglia, located deep within the brain. It is responsible for the regulation of motor control and movement.', 'The globus pallidus is found in the basal ganglia of the brain.', 'The globus pallidus is found deep within the brain', 'The globus pallidus is located in the basal ganglia.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36418626",
"http://www.ncbi.nlm.nih.gov/pubmed/26917269",
"http://www.ncbi.nlm.nih.gov/pubmed/31927758",
"http://www.ncbi.nlm.nih.gov/pubmed/7133405",
"http://www.ncbi.nlm.nih.gov/pubmed/14614896",
"http://www.ncbi.nlm.nih.gov/pubmed/2428943",
"http://www.ncbi.nlm.nih... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36724759",
"endSection": "abstract",
"offsetInBeginSection": 277,
"offsetInEndSection": 522,
"text": "This pilot study was conducted in 4 patients with Parkinson's disease (PD) who underwent MRI-guided deep brain s... | 13 | BioASQ-training13b | null | null | 662cfbf5187cba990d000007 |
factoid | What is the approximate prevalence of autoimmune diseases? | ['10%'] | ["Autoimmune diseases affect approximately 10% of the population, with a higher prevalence in females (about 64% of diagnosed individuals are female). Some of the most common autoimmune diseases, such as Sjögren's syndrome, systemic lupus erythematosus, and systemic sclerosis, are often associated with each other.", 'There is an approximate incidence of 10% autoimmune diseases affecting the general population.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37156255"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37156255",
"endSection": "abstract",
"offsetInBeginSection": 243,
"offsetInEndSection": 313,
"text": "incidence and prevalence of 19 of the most common autoimmune diseases "
},
{
"beginSection": "abstract",... | 13 | BioASQ-training13b | null | null | 66151045fdcbea915f000048 |
factoid | What is the gold standard for a diagnosis of narcolepsy? | ['Sleep study including overnight polysomnography'] | ['The gold standard for diagnosing narcolepsy is a combination of overnight polysomnography (PSG) followed by a multiple sleep latency test (MSLT). PSG is used to rule out other sleep disorders, while the MSLT assesses daytime sleepiness and the presence of sleep-onset REM periods, which are characteristic of narcolepsy. Measuring cerebrospinal fluid hypocretin-1 levels can provide additional diagnostic information.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/12659360",
"http://www.ncbi.nlm.nih.gov/pubmed/37672382"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12659360",
"endSection": "abstract",
"offsetInBeginSection": 688,
"offsetInEndSection": 839,
"text": "referral to an accredited sleep laboratory for a formal sleep study including overnight polysomnography is neces... | 13 | BioASQ-training13b | null | null | 66156200fdcbea915f00004d |
factoid | Which receptor tyrosine kinase is commonly mutated or amplified in pediatric glioma cases? | ['PDGFRA', 'Platelet derived growth factor-alpha', 'Platelet derived growth factor-alpha (PDGFRA)'] | ['Pediatric high-grade glioma (pHGG), including both diffuse midline glioma (DMG) and non-midline tumors, continues to be one of the deadliest oncologic diagnoses. Targeted therapy options aimed at key oncogenic receptor tyrosine kinase (RTK) drivers using small-molecule RTK inhibitors have been extensively studied, but the absence of proper in vivo modeling that recapitulates pHGG biology has historically been a research challenge. Over 20% of pHGG have been found in sequencing studies to have alterations in platelet derived growth factor-alpha (PDGFRA), making growth factor modeling and inhibition via targeted tyrosine kinases a promising research direction.', 'Receptor tyrosine kinase (RTK) alterations are commonly found in pediatric high-grade glioma (pHGG), including diffuse midline glioma (DMG) and non-midline tumors. Sequencing studies have revealed that over 20% of pHGG cases have alterations in platelet derived growth factor-alpha (PDGFRA). This has made growth factor modeling and inhibition via targeted tyrosine kinases a significant area of interest in pHGG research. The challenge in this field has been the lack of proper in vivo modeling that accurately represents pHGG biology.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26727948",
"http://www.ncbi.nlm.nih.gov/pubmed/27582545",
"http://www.ncbi.nlm.nih.gov/pubmed/35978801",
"http://www.ncbi.nlm.nih.gov/pubmed/23970477",
"http://www.ncbi.nlm.nih.gov/pubmed/26744350",
"http://www.ncbi.nlm.nih.gov/pubmed/20479398",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35978801",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Pediatric high-grade glioma (pHGG), including both diffuse midline glioma (DMG) and non-midline tumors, continues ... | 13 | BioASQ-training13b | null | null | 6630390b187cba990d000035 |
factoid | What is the race with the highest incidence of colorectal cancer? | ['Black', 'Black Americans', 'Afroamerican', 'African Americans', 'Blacks', 'African-Americans', 'African americans and African descent'] | ['Based on the provided snippets, it is clear that Black Americans have the highest incidence and mortality from colorectal cancer (CRC). The data indicates that Blacks continued to have the highest incidence of CRC for every age group. Therefore, the answer to the question is that Blacks or African Americans have the highest incidence of colorectal cancer. This highlights a significant health disparity in the US, emphasizing the need for targeted interventions and increased awareness about CRC screening and prevention in this population.', 'African Americans have the highest incidence of colorectal cancer in the United States, with a younger mean age at diagnosis and greater proportion of proximal cancers compared to whites. Survival rates are also lower for African Americans with this type of cancer. Socioeconomic, lifestyle, and healthcare factors do not fully explain the racial disparity, suggesting other etiologic factors may be important in Black American populations.', 'The race with the highest incidence of colorectal cancer is African Americans, particularly African American females. This was found in a study that analyzed data from the Surveillance, Epidemiology, and End Results Registry (SEER) of individuals aged 45-79 years from 2000-2017. The results showed that while the incidence of colorectal cancer decreased for both males and females during the study period, African Americans had the least decline in incidence. Moreover, African American females had the highest risk for colorectal cancer compared to other females or males from different racial groups, and they also had the poorest 5-year survival rate among females. This highlights the need for targeted interventions and screening strategies to reduce the burden of colorectal cancer in this population.', 'The race with the highest incidence of colorectal cancer is African Americans, who have the highest colorectal cancer incidence and mortality rates of any U.S. racial/ethnic group. This disparity exists despite efforts to promote awareness and screening, and is not fully explained by established risk factors or socioeconomic status. In fact, researchers are actively seeking to understand other etiologic factors that may contribute to this health disparity. Additionally, African Americans with colorectal cancer tend to be diagnosed at a younger age and have more proximal cancers compared to whites, further highlighting the need for targeted interventions to reduce this health disparity.', 'Colorectal cancer is the third most common cancer diagnosed in both men and women in the United States and is the second leading cause of cancer death. According to the most recent data, African Americans had the highest incidence rate among all races.', 'According to the provided information, Black Americans have the highest incidence of colorectal cancer compared to other racial groups. The abstracts state that "Black Americans demonstrat[e] the highest incidence and mortality from this disease" and "blacks continued to have the highest incidence of CRC for every age group."', 'Black Americans demonstrating the highest incidence and mortality from this disease', 'According to the provided information, Black Americans have the highest incidence of colorectal cancer compared to other racial groups. The passages state that "Black Americans demonstrat[e] the highest incidence and mortality from this disease" and "blacks continued to have the highest incidence of CRC for every age group."', 'Summary: Black Americans exhibit the highest incidence and mortality rates from colorectal cancer (CRC) compared to other races in the United States. This highlights a significant health disparity, emphasizing the need for targeted interventions and increased awareness about CRC screening and prevention among this population.', 'Black Americans have the highest incidence and mortality rate from colorectal cancer (CRC) compared to other racial groups. This was observed across all age groups.', 'The race with the highest incidence of colorectal cancer (CRC) is Black Americans. This has been consistently observed across different age groups. The incidence of CRC among Black Americans is persistently higher compared to other racial groups, making them the most affected demographic in terms of CRC occurrence.', ' Africans, certain genetic, lifestyle, and clinical factors may contribute to a higher incidence of colorectal cancer in specific populations, but the overall risk is influenced by a complex interplay of various factors and may vary among individuals within each population. Early diagnosis and prompt initiation of appropriate cancer treatments are essential for reducing morbidity and improving outcomes. ', 'Black Americans have the highest incidence of colorectal cancer (CRC) compared to other racial and ethnic groups in the United States. This is consistent across various studies and sources, which show that CRC incidence and mortality rates are significantly higher in Black Americans compared to non-Hispanic Whites, Hispanics, Asian/Pacific Islanders, and Native Americans. The disparity in CRC incidence and mortality rates between Black Americans and other racial and ethnic groups is likely due to a combination of genetic, environmental, and socioeconomic factors. It is important to continue researching and addressing these disparities to improve CRC outcomes for all populations.', 'Summary: Black Americans have the highest incidence of colorectal cancer (CRC) in the United States across all age groups. The disparity is multifactorial and includes societal issues, environmental factors, and immune or genetic changes. While prevention through screening mitigates disparities before CRC develops, further research is needed to understand these differences fully.', 'The race with the highest incidence of colorectal cancer is non-Hispanic Black service members, but this study observed similar rates of colorectal cancer for all races and ethnicities after adjusting for age.', 'Black Americans have the highest incidence of colorectal cancer (CRC) compared to other racial/ethnic groups in the United States. This is supported by multiple studies and sources, including a 2016 report stating that CRC incidence was higher among Blacks (42.5 per 100,000) than Whites (38.0), Latinos (31.7) and Asians (30.0). Additionally, a 2012 study found that after a mean follow-up of 10.8 years, CRC incidence was the highest in African-Americans (annualized rate = 0.14%) compared to Whites, Native Americans, Asian/Pacific Islanders, and Hispanics. A 2021 study also found that Black Americans have a higher risk of CRC incidence and mortality compared to other groups.', 'The race with the highest incidence of colorectal cancer is African Americans (AAs). This racial group has been consistently shown to have higher rates of colorectal cancer incidence and mortality compared to other races in the United States. The disparity between AAs and Non-Hispanic Whites (NHWs) is multifactorial, including genetic, environmental, and societal factors. Some studies suggest that interventions such as increasing screening utilization rates among AAs to match NHWs can help reduce this incidence disparity. Additionally, research has identified unique genetic and epigenetic changes in AA colorectal cancers, which could lead to more precise approaches to colorectal cancer care for this population. Despite these findings, there is still a need for a better understanding of the etiologic factors contributing to the higher incidence and mortality rates of colorectal cancer among African Americans.', 'Summary: African Americans have the highest incidence of colorectal cancer in the United States with a younger mean age at diagnosis and lower survival rates compared to whites. Socioeconomic, lifestyle, and healthcare factors do not fully explain this disparity.', 'The race with the highest incidence of colorectal cancer (CRC) in the United States is Black Americans. This was observed across all age groups, with no decrease in incidence seen in any age group in 2016. The disparity in CRC incidence and mortality between racial and ethnic groups appears to be multifactorial, with structured societal issues, abnormal environmental factors, and cancer-specific immune and genetic changes contributing to the observed differences. Although acquiring additional knowledge into the science behind these disparities is crucial for developing interventions that reduce both CRC incidence and mortality, current evidence suggests that prevention through CRC screening has been effective in mitigating the disparity, but only before CRC has developed.', 'According to the provided information, African Americans have the highest incidence rates of colorectal cancer compared to other racial and ethnic groups in the United States. The data consistently shows that colorectal cancer incidence is significantly higher in African Americans than in non-Hispanic whites, Hispanics, Asian/Pacific Islanders, and other racial groups. African Americans are about 20% more likely to get colorectal cancer and 40% more likely to die from it than most other groups.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/16532978",
"http://www.ncbi.nlm.nih.gov/pubmed/15184825",
"http://www.ncbi.nlm.nih.gov/pubmed/38082093",
"http://www.ncbi.nlm.nih.gov/pubmed/22791544",
"http://www.ncbi.nlm.nih.gov/pubmed/15743345",
"http://www.ncbi.nlm.nih.gov/pubmed/12716038",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34148614",
"endSection": "abstract",
"offsetInBeginSection": 123,
"offsetInEndSection": 206,
"text": "Black Americans demonstrating the highest incidence and mortality from this disease"
},
{
"beginSection"... | 13 | BioASQ-training13b | null | null | 66214c5db9f8b89d7e000002 |
factoid | LRP6 is a member of what superfamily of cell-surface receptors? | ['Low Density lipoprotein receptors'] | ['LRP6 is a member of the low-density lipoprotein receptor superfamily of cell-surface receptors.', 'LRP6 is a member of the low-density lipoprotein receptor (LDLR) superfamily of cell-surface receptors.', 'LRP6 is a member of the low-density lipoprotein (LDL) receptor superfamily of cell-surface receptors.', 'LRP6 (low-density lipoprotein receptor-related protein 6) is a member of the LDL receptor superfamily that plays an important role in regulating the Wnt/β-catenin signaling pathway.', 'LRP6 is a member of the low-density lipoprotein receptor superfamily of cell-surface receptors', 'LRP6 is a member of the low-density lipoprotein receptor superfamily.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/35052459",
"http://www.ncbi.nlm.nih.gov/pubmed/26046396",
"http://www.ncbi.nlm.nih.gov/pubmed/16263759",
"http://www.ncbi.nlm.nih.gov/pubmed/16390319",
"http://www.ncbi.nlm.nih.gov/pubmed/28966723",
"http://www.ncbi.nlm.nih.gov/pubmed/9704021",
"http://www.ncbi.nlm.ni... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35052459",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "LRP6 is a member of the low-density lipoprotein receptor superfamily of cell-surface receptors. "
},
{
"beg... | 13 | BioASQ-training13b | null | null | 662cfd21187cba990d000009 |
factoid | What are episignatures? | ['unique genomic DNA methylation patterns'] | ['Episignatures are genomic DNA methylation patterns that are associated with specific diseases, such as Duchenne Muscular Dystrophy. These patterns can be used for diagnostic testing and as disease biomarkers.', 'Episignatures are unique genomic DNA methylation patterns that can be used for diagnostic testing and as disease biomarkers', 'Episignatures are a type of epigenetic signature that refers to specific patterns of DNA methylation and histone modifications that are associated with certain genetic disorders.', 'Episignatures are distinct, highly sensitive, and specific biomarkers that have recently been applied in clinical diagnosis of genetic syndromes.', 'Episignatures are unique genomic DNA methylation patterns associated with certain genetic syndromes. They can be used for diagnostic testing and as disease biomarkers.', 'Episignatures are unique genomic DNA methylation patterns that can be used for diagnostic testing and as disease biomarkers.', 'Episignatures are unique genomic DNA methylation patterns that are associated with genetic syndromes and can be used for diagnostic testing and as disease biomarkers', 'Episignatures are unique genomic DNA methylation patterns that have been associated with a growing number of genetic syndromes. These DNA methylation patterns can be used for diagnostic testing and as disease biomarkers.', 'Episignatures refer to unique genomic DNA methylation patterns that have been associated with a growing number of genetic syndromes. These episignatures can be used for diagnostic testing and as disease biomarkers.', 'Episignatures are unique genomic DNA methylation patterns that can be used for diagnostic testing and as disease biomarkers in genetic syndromes.', 'Episignatures are unique genomic DNA methylation patterns.', 'Episignatures are unique genomic DNA methylation patterns. They are associated with various genetic syndromes and can be used for diagnostic testing and as disease biomarkers', 'Episignatures are distinct, highly sensitive, and specific biomarkers that represent unique genomic DNA methylation patterns.', 'Episignatures are unique genomic DNA methylation patterns that have been associated with a growing number of genetic syndromes. They can be used for diagnostic testing and as disease biomarkers.', 'Episignatures refer to unique genomic DNA methylation patterns that have been associated with certain genetic syndromes. These episignatures can be used for diagnostic testing and as disease biomarkers.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36572586"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36572586",
"endSection": "abstract",
"offsetInBeginSection": 548,
"offsetInEndSection": 744,
"text": "A growing number of genetic syndromes have been associated with unique genomic DNA methylation patterns (called ... | 13 | BioASQ-training13b | null | null | 66301e04187cba990d000027 |
factoid | What are the clinical indication for Transarterial Chemoembolization (TACE) in liver metastasis for colorectal cancer? | ['Unresectable chemotherapy refractory liver metastasis when conventional therapies fail', 'Liver dominant metastasis', 'liver metastases not amenable to curative surgical resection'] | ["Transarterial chemoembolization (TACE) is a locoregional therapy used in the palliative treatment of primary and secondary hepatic malignancies, including colorectal cancer liver metastases (CRLM). TACE involves the injection of a chemotherapeutic agent and embolic material into the hepatic artery, which supplies blood to the liver tumors. This results in a high concentration of the chemotherapeutic agent within the tumor, while minimizing systemic exposure and associated side effects. TACE can be used as a bridge to surgery, downstaging of unresectable tumors, or as a palliative treatment for patients with unresectable or recurrent CRLM. The use of TACE in CRLM has been shown to improve overall survival and progression-free survival in some studies, but its role in the management of CRLM remains controversial. The decision to use TACE in CRLM should be individualized and based on the patient's clinical presentation, tumor burden, and liver function.", "TACE is a treatment option for liver metastasis in colorectal cancer, especially when surgical resection is not possible. It is typically used when both lobes of the liver are involved, making surgical resection impossible. In selected cases, chemotherapy may be given systemically or via the hepatic artery. The effectiveness and safety of percutaneous ethanol injection, another treatment option, are not well established. The prognosis for colorectal cancer depends on various factors, including the stage of the cancer, the person's overall health, and the success of treatment.", 'Transarterial Chemoembolization (TACE) is indicated for liver metastasis in colorectal cancer when conventional therapies fail, metastases recurrence occurs, or the cancer is unresectable and refractory to chemotherapy. It is particularly effective for larger, intermediate (3-5 cm) lesions.', 'Transarterial Chemoembolization (TACE) in liver metastasis for colorectal cancer is clinically indicated for colorectal liver metastases, unresectable chemotherapy refractory CRCLM, and liver-dominant colorectal liver metastases.', 'Transarterial Chemoembolization (TACE) is a treatment option for liver metastasis from colorectal cancer when conventional therapies fail or metastases recurrence occurs. It is well tolerated and effective in patients with unresectable chemotherapy refractory liver metastases', 'Transarterial chemoembolization (TACE) is an interventional radiologic procedure in which chemotherapeutic agents and embolic materials are injected through the hepatic artery for the treatment of liver malignancies, including metastatic colorectal cancer (mCRC). TACE is considered when surgical resection is not possible or if the metastases are limited to the liver and confined to one lobe.', "Transarterial Chemoembolization (TACE) is not specifically mentioned as a clinical indication for liver metastasis of colorectal cancer in the provided articles. The general treatment for colorectal cancer with liver metastasis includes surgery, radiation therapy, chemotherapy, and targeted therapy. The choice of treatment depends on the stage and location of the cancer, as well as the patient's overall health. Chemotherapy is often used in stages III and IV of colon cancer, and it can include capecitabine, fluorouracil, irinotecan, oxaliplatin, and UFT. For rectal cancer, chemoradiotherapy is often used in conjunction with chemotherapy in a neoadjuvant fashion to enable surgical resection. Immunotherapy with immune checkpoint inhibitors has been found to be useful for a type of colorectal cancer with mismatch repair deficiency and microsatellite instability. Palliative care is recommended for any person who has advanced colon cancer or who has significant symptoms.\n\nTACE is a procedure that is well tolerated and effective in patients with unresectable chemotherapy refractory liver tumors, but it is not specifically mentioned as a clinical indication for liver metastasis of colorectal cancer.", 'TACE is a treatment option for liver metastasis in colorectal cancer, typically used when both lobes of the liver are involved, making surgical resection impossible. It is a minimally invasive procedure that involves injecting chemotherapy drugs directly into the artery that supplies blood to the tumor, followed by embolization to block the blood flow to the tumor. The aim is to shrink the tumor and improve symptoms. In selected cases, chemotherapy may be given systemically or via the hepatic artery. The effectiveness and safety of percutaneous ethanol injection, another treatment option, are not well established.', 'The main clinical indications for using Transarterial Chemoembolization (TACE) in liver metastases from colorectal cancer are:\n\n1. When the liver metastases are unresectable or not amenable to curative surgical resection\n2. As a palliative treatment for chemotherapy-refractory liver metastases to reduce tumor burden, slow progression, and improve quality of life\n3. When conventional therapies fail or metastatic recurrence occurs\n\nTACE is generally well tolerated but may be less effective for larger metastatic lesions (3-5 cm). It allows delivery of high-dose chemotherapy directly to liver tumors while sparing normal liver tissue.', 'Transarterial chemoembolization (TACE) is increasingly used for patients with liver-dominant colorectal metastases after failure of surgery or systemic chemotherapy. It can potentially be used for pre- and post-operative downsizing, minimizing time-to-surgery, and prolongation of overall survival after surgery in patients with colorectal liver only metastases. However, it is not currently recommended as a standard treatment for colorectal liver metastases.', 'Transarterial Chemoembolization (TACE) is indicated for liver metastasis in colorectal cancer patients when conventional therapies fail, or metastases recurrence occurs. It is particularly effective and well-tolerated in patients with unresectable chemotherapy refractory.', 'The clinical indications for Transarterial Chemoembolization (TACE) in liver metastasis for colorectal cancer are unresectable and chemorefractory liver metastases. TACE is considered when systemic therapy has failed, and surgical resection is not possible. The goal of TACE is to prolong survival and palliate symptoms. It can be used as a standalone treatment or in combination with other local or systemic therapies. Conventional TACE (cTACE) and DEBIRI-TACE are two types of chemoembolization that have shown comparable results in different clinical settings, although the evidence is not yet definitive due to variations in study populations and prior therapies. A multidisciplinary approach is recommended to offer patients the best possible care.', 'TACE clinical indications for liver metastases from colorectal cancer include unresectable lesions, chemo-refractory disease, post-conventional therapy recurrence, and intermediate-sized (3-5 cm) tumors with poor local control rates and overall survival. TACE is a well-tolerated alternative to systemic chemotherapy for these patient populations.', 'Transarterial Chemoembolization (TACE) is a minimally invasive treatment for liver metastasis of colorectal cancer. TACE is a combination of chemotherapy and embolization of the hepatic artery, which is the main blood supply of the liver. The clinical indication for TACE in liver metastasis of colorectal cancer is the presence of unresectable liver metastasis, which is defined as liver metastasis that cannot be removed by surgery. TACE is used to treat liver metastasis that is unresectable or has failed to respond to previous treatments. The treatment is usually performed in patients with advanced colorectal cancer that has spread to the liver, and it can be used as a palliative treatment to relieve symptoms such as pain and bleeding. TACE can also be used as a neoadjuvant treatment before surgery to reduce the size of liver metastasis and improve the chances of successful surgical resection.', 'Transarterial Chemoembolization (TACE) is a minimally invasive treatment option for liver metastasis from colorectal cancer when conventional therapies fail or metastases recurrence occurs. It involves the delivery of chemotherapy drugs directly to the tumor through a catheter inserted into the hepatic artery, while simultaneously blocking the blood supply to the tumor. This combination of chemotherapy and embolization can help to reduce the size of the tumor and improve patient outcomes', 'Transarterial Chemoembolization (TACE) is indicated for liver metastases from colorectal cancer that are unresectable and refractory to chemotherapy, especially when lesions are larger (3-5 cm) and conventional therapies have failed or metastases recur.', "TACE is indicated for colorectal cancer liver metastases when the disease is unresectable, refractory to chemotherapy, or recurrent after conventional treatments. It's also considered for intermediate-sized lesions with poor local control and overall survival rates, providing an alternative treatment option to systemic chemotherapy.", 'Based on the provided abstracts, Transarterial Chemoembolization (TACE) is a treatment option for unresectable colorectal cancer with liver metastasis (CRCLM). The clinical indications for TACE in liver metastasis for colorectal cancer are: , 1. Unresectable liver metastases: TACE can be used to treat patients who are not eligible for surgical resection of their liver metastases., 2. Failure of systemic therapy: TACE can be considered as an additional treatment option after the failure of first-line, second-line, third-line, or fourth-line systemic chemotherapy and targeted therapy. , In these situations, TACE with drug-eluting beads (DEB-TACE) combined with systemic chemotherapy and targeted therapy may lead to a favorable disease control rate and survival outcomes in patients with CRCLM.', 'Transarterial Chemoembolization (TACE) is a minimally invasive treatment for liver metastasis of colorectal cancer. TACE is a combination of chemotherapy and embolization of the hepatic artery, which is the main blood supply of the liver. The clinical indication for TACE in liver metastasis of colorectal cancer is the presence of unresectable liver metastasis, which is defined as liver metastasis that cannot be removed by surgery. TACE is used to treat liver metastasis that is unresectable or has progressed after previous treatment with surgery or chemotherapy. TACE is also used to relieve symptoms such as pain and bleeding in patients with liver metastasis. The response to TACE is evaluated by imaging studies such as CT or MRI, and the response is usually evaluated after 2-3 months of treatment. The minimum molecular determinations necessary for the initial treatment of advanced colorectal cancer in clinical practice are the presence of unresectable liver metastasis, the absence of metastasis in other organs, and the presence of a KRAS mutation. The role of epiregulin and amphiregulin in the use of EGFR inhibitors for colorectal cancer is to promote the progression of colorectal cancer by activating the EGFR signaling pathway. The clinical management and outcomes of patients with liver metastasis of colorectal cancer treated with TACE are affected by the subtype of volvulus, which is classified into three subtypes based on the X-ray signs and CT features. The subtype of volvulus is correlated with the clinical management and outcomes of patients with liver metastasis of colorectal cancer.', 'Transarterial chemoembolization (TACE) is a therapeutic option for patients with colorectal cancer liver metastasis who are not candidates for curative treatments. It has been shown to improve the prognosis of these patients.', 'Dummy', 'TACE is an option for unresectable colorectal cancer liver metastases when conventional therapies fail or recurrence occurs, indicated by: 1) Unresectable liver-only mets, 2) failure of systemic chemo (progression on at least two lines), 3) presence of predominantly liver disease, and 4) absence of significant extrahepatic spread. It can be used alone or with other therapies in a multidisciplinary approach for individual patient strategies.', 'Transarterial Chemoembolization (TACE) is typically indicated for patients with unresectable liver metastasis from colorectal cancer that is refractory to chemotherapy. This means that the cancer has not responded to conventional chemotherapy treatments. TACE is often considered when other therapies fail or when metastases recurrence occurs', "The key clinical indications for using transarterial chemoembolization (TACE) in colorectal cancer liver metastases are:\n\n1) When the liver metastases are not amenable to curative surgical resection \n2) As a palliative treatment to reduce tumor burden and symptoms\n3) To deliver high-dose chemotherapy directly to liver tumors while sparing normal liver tissue\n\nTACE is used as a minimally invasive, palliative treatment for colorectal liver metastases that cannot be surgically removed. It works by blocking the tumor's blood supply and delivering chemotherapy locally to the tumor, resulting in higher drug concentrations in the tumor for a longer time compared to the rest of the liver. However, TACE is not a curative treatment for metastatic colorectal cancer.", '1. Symptom palliation in unresectable cases.\n2. Tumor downsizing prior to surgery.\n3. Bridge to surgery.\n4. Control of tumor growth.', 'Transarterial chemoembolization (TACE) is a treatment modality for liver metastasis for colorectal cancer. It is used for patients with unresectable liver metastasis, and it is a palliative treatment for patients with liver metastasis that is not amenable to surgical resection. TACE is a minimally invasive procedure that involves the delivery of chemotherapy directly to the liver through the hepatic artery. It has been shown to be effective in improving survival and quality of life in patients with liver metastasis from colorectal cancer.', "Transarterial Chemoembolization (TACE) is an alternative treatment for unresectable colorectal cancer liver metastasis (CRCLM). Clinical indications include: 1) Unresectable liver metastases, where TACE can be used when surgery isn't possible; and 2) Failure of systemic therapy, making it a potential option after chemotherapy or targeted treatment. In these cases, using DEB-TACE with other treatments may improve disease control and survival rates in CRCLM patients.", 'Transarterial chemoembolization (TACE) is a treatment modality for liver metastasis of colorectal cancer. It is used for patients with unresectable liver metastasis, and it is effective in improving survival time and quality of life.', "The main indications for TACE are:\n* Unresectable or transiently resectable colorectal liver metastases\n* Achieving stable disease after initial chemotherapy\n* Improvement of the patient's performance status\n* To obtain a tumor response or to downstage the tumor burden before a planned curative surgery\n* To treat lesions that do not respond to systemic chemotherapy\n* To treat tumor recurrence after liver resection", 'Transarterial Chemoembolization (TACE) in liver metastasis for colorectal cancer is well-tolerated and effective in patients with unresectable chemotherapy refefractory (larger intermediate (3-5 cm), when conventional therapies fail, or metastases recurrence occurs..', 'Transarterial Chemoembolization (TACE) is a well-tolerated and effective treatment option for patients with unresectable, chemotherapy-refractory liver metastases from colorectal cancer. It is particularly beneficial for larger, intermediate (3-5 cm) lesions, where local control rates and overall survival are relatively worse.', '1. Symptomatic control of intrahepatic tumor burden, particularly in patients with unresectable, or progressive disease 2. Liver-dominant metastases, in the absence of extrahepatic disease 3. Improving patient survival 4. Bridge to transplant in selected patients 5. Downsizing of liver lesion in preparation for resection in selected patients.', 'The clinical indications for Transarterial Chemoembolization (TACE) in liver metastasis for colorectal cancer include: * Unresectable liver metastases * Chemotherapy refractory disease * Recurrence of metastases after conventional therapies * Intermediate-sized lesions (3-5 cm) with poor local control rates and overall survival , TACE is a well-tolerated and effective treatment option in these patient populations, offering an alternative to systemic chemotherapy.', 'TACE is indicated for patients with unresectable, chemotherapy-refractory liver metastases from colorectal cancer. \n\nPlease provide your answer in a concise and clear manner. \nPlease note that you should not provide any additional information beyond what is provided in the context. \nPlease also note that you should not provide any information that is not supported by the context. \nPlease be accurate and precise in your answer. \nPlease be polite and respectful in your tone. \nPlease be patient and understanding in your response. \nPlease be aware that you are a biomedical question answering assistant, and you should provide answers based on the context provided. \nPlease be aware that you should not provide any personal opinions or biases in your answer. \nPlease be aware that you should not provide any information that is not supported by the context. \nPlease be aware that you should not provide any information that is not accurate or precise. \nPlease be aware that you should be polite, respectful, patient, and understanding in your response. \nPlease be aware that you are a biomedical question answering assistant, and you should provide answers based on the context provided. \nPlease be aware that you should not provide any personal opinions or biases in your answer. \nPlease be aware that you', 'Transarterial Chemoembolization (TACE) in liver metastasis for colorectal cancer is indicated for the treatment of CRLM using irinotecan-loaded microspheres in patients with colorectal cancer.', 'Based on the provided abstracts, Transarterial Chemoembolization (TACE) is a viable option for patients with unresectable liver metastases from colorectal cancer who have failed or are refractory to systemic chemotherapy. The clinical indications for TACE in liver metastasis for colorectal cancer include: * Unresectable liver metastases * Failure or refractoriness to systemic chemotherapy * Palliation of symptoms related to liver metastases , TACE can be used as a salvage therapy to control local metastases and improve survival time. The procedure involves the local injection of a combination of chemotherapeutic and embolic agents, which can be tailored to individual patients based on their clinical setting and prior therapies.', 'The clinical indication for Transarterial Chemoembolization (TACE) in liver metastasis for colorectal cancer is unresectable chemotherapy refractory liver metastasis, particularly for larger, intermediate (3-5 cm) lesions.', 'Transarterial Chemoembolization (TACE) is indicated for unresectable chemotherapy refractory liver metastases, particularly in cases of colorectal cancer.', 'There is no clear indication for Transarterial Chemoembolization (TACE) in liver metastasis for colorectal cancer, but it is increasingly used for patients with liver-dominant metastases after failure of surgery or systemic chemotherapy as a valuable option for pre- and post-operative downsizing, minimizing time-to-surgery, and prolongation of overall survival after surgery.', "Transarterial Chemoembolization (TACE) is not specifically mentioned as a clinical indication for liver metastasis of colorectal cancer. However, TACE is a treatment option for liver tumors, including metastases from colorectal cancer. It is a minimally invasive procedure that delivers chemotherapy drugs directly to the liver tumor through the hepatic artery, blocking the blood supply to the tumor and reducing its growth. The use of TACE in liver metastasis of colorectal cancer may depend on the patient's overall health, the extent of the cancer, and the presence of other medical conditions. Other treatment options for liver metastasis of colorectal cancer include surgery (hepatectomy), chemotherapy, and therapies specifically aimed at the liver like radiofrequency ablation, selective internal radiation therapy, and irreversible electroporation.", 'TACE is indicated for patients with unresectable liver metastases and chemotherapy refractory colorectal cancer.', 'TACE is well tolerated and effective in patients with unresectable chemotherapy refractory liver metastasis for colorectal cancer'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/30190956",
"http://www.ncbi.nlm.nih.gov/pubmed/24451734",
"http://www.ncbi.nlm.nih.gov/pubmed/32468211",
"http://www.ncbi.nlm.nih.gov/pubmed/32620520",
"http://www.ncbi.nlm.nih.gov/pubmed/25444473",
"http://www.ncbi.nlm.nih.gov/pubmed/34318754",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35326651",
"endSection": "abstract",
"offsetInBeginSection": 395,
"offsetInEndSection": 551,
"text": "vascular- and image-based treatments offered by interventional radiologists have emerged when conventional thera... | 13 | BioASQ-training13b | null | null | 662fbec6187cba990d00000f |
factoid | What is the prevalence of intellectual developmental disorders in Duchenne Muscular Dystrophy? | ['22%'] | ['The prevalence of intellectual developmental disorders in Duchenne Muscular Dystrophy (DMD) is approximately 22%.', 'The prevalence of intellectual developmental disorders in Duchenne Muscular Dystrophy is 22%.', 'The prevalence of intellectual developmental disorder (IDD) in Duchenne muscular dystrophy (DMD) is 22%.', 'The prevalence of intellectual developmental disorders in Duchenne muscular dystrophy is 22%', 'The prevalence of intellectual developmental disorders (IDD) in Duchenne Muscular Dystrophy (DMD) is 22%.', 'The global prevalence of intellectual developmental disorder (IDD) is 22% in Duchenne muscular dystrophy (DMD).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36440509"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36440509",
"endSection": "abstract",
"offsetInBeginSection": 1369,
"offsetInEndSection": 1517,
"text": "The global prevalence of intellectual developmental disorder (IDD) was 8% in Becker muscular dystrophy and 22%... | 13 | BioASQ-training13b | null | null | 66300ee7187cba990d00001c |
factoid | Which tick genus is the vector for Lyme disease? | ['Ixodes'] | ['The tick genus Ixodes is the primary vector for Lyme disease. These ticks are found in various regions of North America and Europe, where they transmit the bacterium Borrelia burgdorferi to humans and other animals.', 'Ixodes is the tick genus that is known to be a vector for Lyme disease. Specifically, Ixodes scapularis, also known as the blacklegged tick or deer tick, is the primary vector of Lyme disease in the United States and Canada. Other species within the Ixodes genus, such as Ixodes holocyclus in Australia, have also been implicated in the transmission of Lyme disease.', 'Ixodes is the tick genus that is the vector for Lyme disease.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36944114",
"http://www.ncbi.nlm.nih.gov/pubmed/37042198",
"http://www.ncbi.nlm.nih.gov/pubmed/36958955"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37042198",
"endSection": "abstract",
"offsetInBeginSection": 316,
"offsetInEndSection": 330,
"text": "Ixodes ricinus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/369... | 13 | BioASQ-training13b | null | null | 660c0071fdcbea915f00002b |
factoid | In what part of the body would a periprosthetic infection occur? | ['near an implant', 'In the area around the prosthetic joint.'] | ['Periprosthetic infections occur in the part of the body where a prosthetic device has been implanted, such as the joint or bone.', 'A periprosthetic infection occurs around the area of an implanted prosthetic, such as in the hip or knee joints following total hip arthroplasty (THA) or total knee arthroplasty (TKA).', 'Periprosthetic infection is a foreign-body-associated infection that is characterised by delayed osteomyelitis of bone tissue surrounding artificial joint replacement.', 'A periprosthetic infection occurs in the area around a prosthetic hip or knee joint.', 'A periprosthetic joint infection (PJI) would occur around a prosthetic joint, such as after a total hip arthroplasty (THA) or total knee arthroplasty (TKA).', 'Periprosthetic infection occurs in the joint space after joint replacement surgery.', 'A periprosthetic infection can occur in the area surrounding an implanted joint prosthesis, such as a total hip or knee replacement.', 'A periprosthetic infection would occur around the area of an artificial joint, such as those implanted during hip or knee replacement surgeries. This includes infections that can develop around hip replacements (THA) and knee replacements (TKA/UKA)', 'A periprosthetic infection occurs around the area of an implanted prosthesis, typically in joints such as the hip or knee.', 'Periprosthetic joint infection (PJI) is a complication of total hip arthroplasty (THA) or total knee arthroplasty (TKA) that occurs due to infection of the joint space.', 'A periprosthetic infection can occur in various parts of the body depending on the type of prosthesis. In the context of total hip arthroplasty, periprosthetic infection can occur around the hip joint. In the context of shoulder arthroplasty, periprosthetic infection can occur around the shoulder joint.', 'A periprosthetic infection would occur in the periprosthetic joint.', 'A periprosthetic infection would occur in the joint where the prosthesis is placed.', 'Periprosthetic infections occur around artificial joints, most commonly in the hip and knee.', 'A periprosthetic joint infection (PJI) occurs in the area surrounding a joint replacement implant, such as a hip or knee replacement. It is an infection that affects the tissues around the prosthetic joint and can lead to serious complications if not treated promptly and effectively.', 'A periprosthetic infection is an infection occurring around a joint prosthesis. These types of infections often occur after total knee and hip arthroplasties.', 'A periprosthetic infection occurs in the joints, specifically in the hip or knee, after a total hip or knee arthroplasty surgery.', 'A periprosthetic infection can occur in the area surrounding a prosthetic joint, such as the hip, knee, or shoulder.', 'A periprosthetic infection would occur in a joint that has been replaced by a prosthesis.', 'A periprosthetic infection would occur in the joint, heart valves, or due to schroeteri.', 'Periprosthetic joint infections (PJI) are infections occurring around a total joint replacement. They could happen around the hip joint (THA) or knee joint (TKA/UKA).', 'Periprosthetic infections occur in the area surrounding the prosthetic joint.', 'A periprosthetic infection occurs in the tissue surrounding a prosthetic joint (i.e. knee or hip replacement).', 'A periprosthetic infection can occur in any part of the body where artificial joint replacement has been performed, such as hip, knee, shoulder, elbow or ankle. It is a foreign-body-associated infection that affects the surrounding tissue of artificial implant.', 'A periprosthetic infection would occur around the area of an artificial joint, such as in the hip or knee, following procedures like total hip arthroplasty (THA) or total and unicompartmental knee arthroplasty (TKA/UKA).', 'A periprosthetic infection can occur in the area surrounding a prosthetic joint, such as the hip or knee.', 'A periprosthetic infection (PJI) is an infection that occurs around a prosthetic joint, such as a knee or hip replacement.', '\nA periprosthetic infection would occur around an artificial joint replacement, such as in the hip, knee, shoulder, elbow, or ankle joint.', 'A periprosthetic infection usually occurs in areas where prosthetics are implanted, such as joints, including the hip and knee.', 'A periprosthetic joint infection (PJI) occurs in the tissues surrounding a prosthetic joint, such as after total hip or knee replacement surgery. The infection can involve the joint space, bone, and soft tissues around the prosthetic implant.', 'A periprosthetic infection would occur in close to a joint or structure in close relation to an implant.', 'A periprosthetic joint infection (PJI) would occur in the joint space of a prosthetic joint.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37887186",
"http://www.ncbi.nlm.nih.gov/pubmed/26135702",
"http://www.ncbi.nlm.nih.gov/pubmed/30374532",
"http://www.ncbi.nlm.nih.gov/pubmed/32238194",
"http://www.ncbi.nlm.nih.gov/pubmed/36200815",
"http://www.ncbi.nlm.nih.gov/pubmed/34142445",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37380142",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 327,
"text": "BACKGROUND: The aim of the present study was to compare causative bacteria and their antibiotic resistance profile... | 13 | BioASQ-training13b | null | null | 66088ffafdcbea915f00000f |
factoid | What is the estimated impact of social determinants of health on health outcomes? | ['Highly significant impact'] | ['The impact of social determinants of health on health outcomes has been extensively studied and it is estimated that these factors play a significant role in shaping health outcomes. For example, studies have shown that people who experience poverty, unemployment, low education levels, poor housing conditions, and limited access to healthy food and safe living environments are more likely to develop chronic diseases, such as diabetes, cardiovascular disease, and mental health disorders. Additionally, social determinants can affect health outcomes indirectly by influencing health behaviors such as smoking, physical inactivity, and unhealthy eating habits. It is estimated that these factors can account for up to 40% of modifiable health risks. Addressing social determinants of health has the potential to improve health equity and reduce health disparities.', 'The social determinants of health have a significant impact on health outcomes, particularly for marginalized populations. Factors such as poverty, lack of education, and living in rural areas can increase the likelihood of adverse health outcomes, including teenage pregnancy and childbearing. According to the World Health Organization, social determinants account for an estimated 30-50% of health inequities. Addressing these factors through targeted interventions and policies can help reduce health disparities and improve overall health outcomes.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37843837",
"http://www.ncbi.nlm.nih.gov/pubmed/37022779",
"http://www.ncbi.nlm.nih.gov/pubmed/35590354",
"http://www.ncbi.nlm.nih.gov/pubmed/29480769",
"http://www.ncbi.nlm.nih.gov/pubmed/20171001",
"http://www.ncbi.nlm.nih.gov/pubmed/27696682",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37501568",
"endSection": "abstract",
"offsetInBeginSection": 658,
"offsetInEndSection": 751,
"text": "social determinants contribute directly and indirectly (through lifestyle) to life expectancy"
},
{
"beg... | 13 | BioASQ-training13b | null | null | 65f86b3ac4010b4d78000058 |
factoid | What is the optimal antiemetic treatment for FOLFIRINOX chemotherapy? | ['5-hydroxytryptamine-3 receptor antagonists (5HT3RA), dexamethasone (DEX), and neurokinin 1 receptor antagonists', '5HT3RA, DEX and NK1RA', '5HT3 receptor antagonist (5HT3RA), dexamethasone (DEX), and a neurokinin-1 receptor antagonist (NK1RA)', 'three-drug regimen with aprepitant'] | ['The optimal antiemetic treatment for FOLFIRINOX chemotherapy includes a three-drug regimen with aprepitant, dexamethasone, and 5-HT3 receptor antagonists. This regimen has been shown to improve the complete response rate during cycle 1 and reduce nausea and vomiting in patients treated with FOLFIRINOX for metastatic pancreatic cancer. However, enhanced antiemetic measures may be necessary as nausea and vomiting can persist beyond 5 days. In patients with diabetes mellitus complications, sparing of steroids and glycemic control should also be considered.', 'The optimal antiemetic treatment for managing side effects from FOLFIRINOX chemotherapy includes a combination of 5-hydroxytryptamine-3 receptor antagonists (5HT3RA), dexamethasone (DEX), and neurokinin 1 receptor antagonists (NK1RA).', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy includes 5HT3RA, DEX, and NK1RA.', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy, which consists of irinotecan, folinic acid, and fluorouracil (5-FU), is a multimodal approach that includes the following:\n\n1. Pregabalin (Lyrica) 150-300 mg orally twice daily starting 1-2 days before chemotherapy and continuing for 3 days.\n\n2. Dexamethasone (Decadron) 8 mg orally or intravenously (IV) twice daily starting 1-2 days before chemotherapy and continuing for 3 days.\n\n3. Palonosetron (Aloxi) 0.25 mg IV or subcutaneously (SC) before chemotherapy.\n\n4. O', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy has not been definitively established. The FOLFIRINOX regimen is known to cause significant nausea and vomiting, and there is a need for effective antiemetic prophylaxis to prevent these adverse events. A study published in the Journal of Clinical Oncology found that a three-drug combination of 5-hydroxytryptamine-3 receptor antagonists (5HT3RA), dexamethasone (DEX), and neurokinin 1 receptor antagonists (NK1RA) was effective in preventing chemotherapy-induced nausea and vomiting (CINV) in patients receiving FOLFIRINOX. However, the study also noted that the optimal antiemetic treatment for FOLFIRINOX may vary depending on patient factors and individual preferences. Other studies have suggested that', 'A three-drug combination of 5-hydroxytryptamine-3 receptor antagonists (5HT3RA), dexamethasone (DEX), and neurokinin 1 receptor antagonists (NK1RA) for the prevention of chemotherapy-induced nausea and vomit during FOLFORINOX therapy', '5-hydroxytryptamine 3 (5-HT3) receptor antagonists are the optimal antiemetic treatments for FOLFIRINOX chemotherapy', 'Based on the given context, the optimal antiemetic treatment for FOLFIRINOX chemotherapy, a standard chemotherapy regimen for advanced pancreatic cancer, should include a combination of 5-hydroxytryptamine-3 receptor antagonists (5HT3RA), dexamethasone (DEX), and neurokinin 1 receptor antagonists (NK1RA) for the prevention of chemotherapy-induced nausea and vomiting (CINV). However, it is important to note that CINV induced by FOLFIRINOX was poorly controlled even with this prophylactic antiemetic therapy, suggesting the need for enhanced antiemetic measures. Additionally, in patients with diabetes mellitus complications, sparing of steroids and glycemic control should be considered due to the risk of hyperglycemia.', '5-HT3RA is a standard antiemetic therapy for FOLFIRINOX chemotherapy. However, patients receiving mFFX are at risk of developing chemotherapy-induced nausea and vomiting (CINV) that is refractory to conventional antiemetic therapy and can persist beyond 5 days. NK1-RA in addition to 5HT3RA and DEX should be used prophylactically to control CINV in mFFX.', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy has not been fully established, and the current standard of care consisting of a three-drug combination of 5-hydroxytryptamine-3 receptor antagonists (5HT3RA), dexamethasone (DEX), and neurokinin 1 receptor antagonists (NK1RA) may not be sufficient to control chemotherapy-induced nausea and vomiting (CINV). Enhanced antiemetic measures, such as additional medications or alternative regimens, may be necessary to improve CINV management for patients undergoing FOLFIRINOX therapy. However, the choice of antiemetic treatment should also consider potential side effects, such as hyperglycemia, and individual patient factors, including diabetes mellitus complications. Further research is needed to determine the most effective and safe antiemetic strategy for FOL', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy is a single oral dose of NEPA (Akynzeo®) plus 12 mg of dexamethasone. NEPA is a fixed-dose combination of netupitant, a neurokinin-1 receptor antagonist (NK1RA), and palonosetron, a 5-hydroxytryptamine type 3 receptor antagonist (5HT3RA), which has been shown to be effective in preventing chemotherapy-induced nausea and vomiting (CINV). This treatment has demonstrated therapeutic benefits in managing and prophylaxis of CINV events, both in naive patients and patients previously treated with serotonin receptor antagonists (5HT3-RA) and neurokinin-1 receptor antagonists (NK1-RA). Additionally, NEPA has been shown to be safe, both before and during the COVID-19 pandemic.', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy is a combination of 5HT3RA, DEX, and NK1RA, with prophylactic therapy starting before the chemotherapy and continuing for at least 5 days after the treatment.', "5HT3RA (5-hydroxytryptamine receptor antagonist), DEX (dexamethasone) and NK1RA (neurokinin-1 receptor antagonist) are commonly used for prophylactic antiemetic therapy in patients undergoing FOLFIRINOX chemotherapy. However, if patient experiences poorly controlled CINV, additional or alternative antiemetic medications should be considered. Olanzapine, aprepitant and other antiemetics could be added to the regimen based on individual patient's needs.", 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy is not specified in the provided context, but it mentions that CINV induced by mFFX was poorly controlled even with prophylactic antiemetic therapy using 5HT3RA, DEX, and NK1RA.', "The optimal antiemetic treatment for FOLFIRINOX chemotherapy includes a combination of multiple drugs. It is recommended to use a 5HT3 receptor antagonist (5HT3RA), dexamethasone (DEX), and a neurokinin-1 receptor antagonist (NK1RA) as prophylactic antiemetic therapy. However, in cases where CINV induced by FOLFIRINOX is poorly controlled even with this standard regimen, additional interventions may be required, such as the use of olanzapine or aprepitant. It is important to individualize the treatment based on the patient's specific needs and response to therapy.", 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy includes prophylactic antiemetic therapy using 5HT3RA, DEX.', "The optimal antiemetic treatment for FOLFIRINOX (mFFX) chemotherapy typically includes a combination of a 5HT3 receptor antagonist (5HT3RA), dexamethasone (DEX), and a neurokinin-1 receptor antagonist (NK1RA). However, it's important to note that even with this prophylactic antiemetic therapy, control of chemotherapy-induced nausea and vomiting (CINV) can be challenging, and symptoms may persist beyond 5 days. This indicates a need for potentially adjusting the treatment approach or exploring additional supportive measures to better manage CINV in patients undergoing this regimen.", 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy is 5-hydroxytryptamine-3 receptor antagonists (5HT3RA), dexamethasone (DEX), and neurokinin 1 receptor antagonists (NK1RA).', ' The optimal antimycin D treatment for FOLFox chemotherapy is not well understood, and there is no one-solution approach that can eliminate the risk of antimycin D-resistance. Instead, there are several strategies that can be employed to mitigate the risk of antimycin D-resistance and improve the efficacy of FOLFox chemotherapy. These strategies include:', '\nAnswer: Aprepitant, dexamethasone, and a 5-HT3 receptor antagonist (granisetron or palonosetron) before and after chemotherapy.', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy has not been definitively established, as various regimens have been used in different clinical trials and real-world settings. However, a few studies suggest that a three-drug combination of 5-hydroxytryptamine-3 receptor antagonists (5HT3RA), dexamethasone (DEX), and neurokinin 1 receptor antagonists (NK1RA) may be effective in preventing chemotherapy-induced nausea and vomiting (CINV) associated with FOLFIRINOX. In a retrospective cohort study of patients with advanced pancreatic cancer, the complete response rate for CINV was 64.7% with this three-drug regimen, although the incidence of nausea and vomiting remained relatively high. Another study found that the addition of aprepitant to', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy has not been fully established, but current guidelines recommend a combination of agents to prevent CINV. The most effective prophylactic regimen typically includes a serotonin receptor antagonist (5HT3RA) such as ondansetron or granisetron, dexamethasone (DEX), and sometimes a neurokinin-1 receptor antagonist (NK1RA) like aprepitant. However, even with this combination therapy, some patients experience persistent nausea and vomiting, highlighting the need for more effective treatments to manage CINV induced by FOLFIRINOX chemotherapy.', "The optimal antiemetic treatment for FOLFIRINOX chemotherapy typically includes a combination of a 5HT3 receptor antagonist (5HT3RA), dexamethasone (DEX), and a neurokinin-1 receptor antagonist (NK1RA). This regimen aims to manage the nausea and vomiting associated with this highly emetogenic chemotherapy. However, it's important to note that even with these medications, control of chemotherapy-induced nausea and vomiting (CINV) can be challenging, and symptoms may persist beyond 5 days. Always consult with a healthcare provider for the most appropriate and individualized treatment plan", 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy is prochlorperazine (PC), a commonly used antiemetic agent. Prochlorperazine (PC), a commonly used antiemetic agent, is the first-line antiemetic agent for patients receiving chemotherapy. Food and liquid restrictions are also', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy includes prophylactic antiemetic therapy using 5HT3 receptor antagonists (5HT3RA), dexamethasone (DEX), and neurokinin-1 receptor antagonists (NK1RA).', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy is a combination of 5HT3RA and DEX.', 'CINV induced by mFFX was poorly controlled even with prophylactic antiemetic therapy using 5HT3RA, DEX, and NK1RA, and was found to persist beyond 5\xa0days', 'The recommended antiemetic treatment for FOLFIRINOX chemotherapy is a combination of 5HT3RA and DEX.', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy is NEPA (netupitant/palonosetron). NEPA has been shown to effectively prevent nausea and vomiting induced by chemotherapy (CINV) in patients receiving FOLFIRINOX and Folfoxiri regimens. This combination of netupitant and palonosetron provides superior control of acute and delayed CINV compared to other antiemetic agents. NEPA can be safely used during the COVID-19 pandemic and has been proven to be effective in real-life studies.', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy includes a combination of 5HT3 receptor antagonists, dexamethasone, and NK1 receptor antagonists.', 'Based on the provided information, chemotherapy-induced nausea and vomiting (CINV) induced by modified FOLFIRINOX (mFFX) chemotherapy was poorly controlled even with prophylactic antiemetic therapy using a combination of a 5-HT3 receptor antagonist (5HT3RA), dexamethasone (DEX), and an NK-1 receptor antagonist (NK1RA). The CINV persisted beyond 5 days.\n\nThe text does not provide information on the optimal antiemetic treatment for FOLFIRINOX. It only indicates that the mentioned antiemetic combination was not fully effective in controlling CINV in this setting. More research would be needed to determine the best approach for managing CINV with this chemotherapy regimen.', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy is a combination of netupitant/palonosetron (NEPA; Akynzeo(®)) with >85% antiemetic efficacy.', '5HT3RA, DEX, and NK1RA', 'The recommended antiemetic treatment for FOLFIRINOX chemotherapy is either 5HT3RA or a combination of 5HT3RA and DEX.', 'The optimal antiemetic treatment for FOLFIRINOX chemotherapy is prochlorperazine (PC), ondansetron (OD), and dexamethasone (Dex) or a combination of these agents.', 'In this study, the researchers found that a three-drug regimen with aprepitant can significantly reduce the incidence of nausea and vomiting in patients with metastatic pancreatic cancer who received FOLFIRINOX chemotherapy.', "The optimal antiemetic treatment for FOLFIRINOX chemotherapy is still a topic of debate. The snippet suggests that prophylactic antiemetic therapy using 5HT3RA, DEX, and NK1RA may not be effective in controlling CINV induced by mFFX. Recent studies suggest that olanzapine may be effective in preventing CINV in patients receiving FOLFIRINOX chemotherapy. However, further research is needed to confirm its efficacy and safety profile. It's essential to consider individual patient factors, such as age, gender, and previous antiemetic response, when choosing an antiemetic regimen.", 'CINV induced by mFFX was poorly controlled even with prophylactic antiemetic therapy using 5HT3RA, DEX, and NK1RA, and was found to persist beyond 5 days.', "The optimal antiemetic treatment for FOLFIRINOX (mFFX) chemotherapy typically includes a combination of a 5HT3 receptor antagonist (5HT3RA), dexamethasone (DEX), and a neurokinin-1 receptor antagonist (NK1RA). However, it's important to note that even with this prophylactic antiemetic therapy, control of chemotherapy-induced nausea and vomiting (CINV) can be challenging, and symptoms may persist beyond 5 days. This indicates a need for potentially adjusting the treatment strategy or exploring additional supportive measures to better manage CINV in patients undergoing this regimen.", '5-hydroxytryptamine 3 receptor (5-HT3R) antagonists and dexamethasone can be used to manage chemotherapy-induced nausea and vomiting in FOLFIRINOX. Other options include neurokinin-1 (NK1) receptor antagonists and other adjunctive medications such as aprepitant, palonosetron and olanzapine.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37884842",
"http://www.ncbi.nlm.nih.gov/pubmed/33023657",
"http://www.ncbi.nlm.nih.gov/pubmed/20413062",
"http://www.ncbi.nlm.nih.gov/pubmed/34131576",
"http://www.ncbi.nlm.nih.gov/pubmed/30019968",
"http://www.ncbi.nlm.nih.gov/pubmed/30333194",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37884842",
"endSection": "abstract",
"offsetInBeginSection": 1255,
"offsetInEndSection": 1408,
"text": "CINV induced by mFFX was poorly controlled even with prophylactic antiemetic therapy using 5HT3RA, DEX, and NK... | 13 | BioASQ-training13b | null | null | 65f7798dc4010b4d78000038 |
factoid | TAK-994 is developed for which disease? | ['narcolepsy'] | ['TAK-994 is an oral orexin receptor 2-selective agonist that was developed and tested for narcolepsy type 1.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37001988",
"http://www.ncbi.nlm.nih.gov/pubmed/37494485"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37494485",
"endSection": "abstract",
"offsetInBeginSection": 93,
"offsetInEndSection": 255,
"text": "METHODS: We conducted a phase 2, randomized, placebo-controlled trial of TAK-994, an oral orexin receptor 2-selec... | 13 | BioASQ-training13b | null | null | 65cfd3961930410b1300001f |
factoid | What disease can be treatment with Bulevirtide? | ['chronic hepatitis D'] | ['Bulevirtide can be used for chronic hepatitis D virus infection.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37943548",
"http://www.ncbi.nlm.nih.gov/pubmed/37929228",
"http://www.ncbi.nlm.nih.gov/pubmed/36113537",
"http://www.ncbi.nlm.nih.gov/pubmed/36377139",
"http://www.ncbi.nlm.nih.gov/pubmed/36192563",
"http://www.ncbi.nlm.nih.gov/pubmed/36196680",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36648369",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "The entry inhibitor bulevirtide (BLV) is a new treatment option for patients with chronic hepatitis D virus (HDV) ... | 13 | BioASQ-training13b | null | null | 65cfdaae1930410b13000025 |
factoid | Which initial chemotherapy regimen is the most appropriate in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients? | ['FOLFOXIRI', 'FOLFIRINOX'] | ['Based on the provided information, both CAPEOX (capecitabine plus oxaliplatin) and FOLFIRINOX appear to be effective induction chemotherapy regimens as part of total neoadjuvant therapy (TNT) for locally advanced rectal cancer.\n\nCAPEOX is mentioned in several studies as the induction chemotherapy given prior to chemoradiotherapy and consolidation chemotherapy. FOLFIRINOX is also noted to have established efficacy, significantly increasing 3-year disease-free survival when used as neoadjuvant therapy.\n\nThe most appropriate regimen may depend on individual patient factors and institutional protocols. However, both CAPEOX and FOLFIRINOX seem to be valid options for induction chemotherapy in the TNT approach for locally advanced rectal cancer patients, with the goal of improving pathologic complete response rates and facilitating delivery of systemic therapy.', 'Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients, the most appropriate initial chemotherapy regimen is mFOLFOXIRI neoadjuvant chemotherapy, which has shown improved pCR rate, survival outcome, and reduced the rate of distant metastasis and anastomotic fistula compared to other regimens.', 'mFOLFOXIRI is the most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients.', 'The most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is mFOLFOXIRI. This regimen has been shown to improve pCR rate and survival outcome, reduce the rate of distant metastasis and anastomotic fistula when compared with mFOLFOX6 neoadjuvant chemotherapy.', 'mFOLFOXIRI', 'In Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients, the mFOLFOXIRI regimen has shown promising results, including improved pathological complete response (pCR) rates, better survival outcomes, reduced distant metastasis rates, and lower incidences of anastomotic fistulas compared to other regimens like mFOLFOX6.', 'The most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is mFOLFOXIRI (modified FOLFOXIRI). This regimen has been shown to improve the pathological complete response (pCR) rate, reduce the rate of distant metastasis, and improve survival outcomes compared to other regimens, such as mFOLFOX6. However, it is important to consider individual patient factors and discuss treatment options with a multidisciplinary team to determine the most suitable regimen for each patient.', 'In Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients, the most appropriate initial chemotherapy regimen could be preoperative induction or consolidation with a range of options such as FOLFOXIRI, FOLFOX, or CAPEOX. However, the decision should be individualized based on patient and tumor characteristics and clinician experience.', "The choice of initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients depends on various factors such as patient's overall health, potential toxicities, and the risk of distant metastasis. Some studies have shown promising results with FOLFOXIRI as the initial chemotherapy regimen in TNT, while others have used TEGAFIRI or CAPOX. However, it is important to note that these studies are still ongoing and their safety and feasibility need to be further evaluated. In Japan, a phase II trial is currently underway to evaluate the safety and activity of a TNT strategy including SCRT, intensified consolidation treatment with FOLFOXIRI and delayed surgery. After protocol amendment, the treatment seems feasible without safety concern. Ultimately, the most appropriate initial chemotherapy regimen in TNT for locally advanced rectal cancer patients will depend on the results of ongoing clinical trials and individual patient characteristics.", 'Based on the provided information, FOLFOXIRI appears to be the most appropriate initial chemotherapy regimen for Total Neoadjuvant Therapy (TNT) in patients with locally advanced rectal cancer. The abstracts mention that FOLFOXIRI is a potential chemotherapy option in the neoadjuvant setting, and that neoadjuvant mFOLFOXIRI regimens improved pathologic complete response (pCR) rate, survival outcomes, and reduced distant metastasis and anastomotic fistula rates compared to mFOLFOX6 neoadjuvant chemotherapy.', 'Neoadjuvant mFOLFOXIRI regimens improved pCR rate and survival outcome, reduced the rate of distant metastasis and anastomotic fistula when comparing with propensity-score matched controls of mFOLFOX6 neoadjuvant chemotherapy.', 'The most appropriate chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is mFOLFOXIRI.', 'In Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients, the most appropriate initial chemotherapy regimen often includes cycles of induction chemotherapy, such as FOLFIRINOX or fluorouracil, leucovorin, and oxaliplatin, followed by chemoradiotherapy to improve pathological complete response rates and facilitate the delivery of chemotherapy before surgery.', 'According to a randomized phase III trial published in The Lancet Oncology in 2018, the most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is mFOLFOXIRI (oxaliplatin, leucovorin, irinotecan, and fluorouracil) followed by short-course radiotherapy (SCRT) and delayed surgery, as compared to the standard of care, which is preoperative radiotherapy (PRT) followed by surgery. The study found that the mFOLFOXIRI-SCRT-surgery arm had a higher pathological complete response (pCR) rate (34% vs 16%) and a lower rate of distant metastases (11% vs 19%) than the PRT-surgery arm. However, the overall survival and local recurrence rates were similar between the two arms. It is essential to note that the decision to use TNT should be individualized based on patient factors and multidisciplinary team discussion.', 'The neoadjuvant mFOLFOXIRI regimen is most appropriate in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients, as it has shown improved pathological complete response rate and survival outcomes, along with reduced rates of distant metastasis and anastomotic fistula.', 'The most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is mFOLFOXIRI (modified FOLFOXIRI). This regimen has been shown to improve pathological complete response (pCR) rates, survival outcomes, and reduce the rate of distant metastasis and anastomotic fistula compared to other regimens like mFOLFOX6. Therefore, mFOLFOXIRI is recommended as the preferred choice for initial chemotherapy in TNT for locally advanced rectal cancer patients.', 'The most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is mFOLFOXIRI.', 'The most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is mFOLFOXIRI. This regimen has been shown to improve pathological complete response (pCR) rates and survival outcomes, as well as reduce the risk of distant metastasis and anastomotic fistula, compared to other neoadjuvant chemotherapy regimens such as FOLFOX or CAPEOX. The mFOLFOXIRI regimen has become a new standard of care for locally advanced rectal cancer patients undergoing TNT.', 'The most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients includes options like FOLFOXIRI, FOLFOX, or CAPEOX, with mFOLFOXIRI showing improved outcomes in some studies.', 'The optimal initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is still not established. However, FOLFOXIRI (5-fluorouracil, leucovorin, oxaliplatin, and irinotecan) appears to be a promising option as suggested by some studies. The decision should be individualized and discussed with patients.', 'The most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is FOLFOXIRI.', 'The most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is induction chemotherapy followed by chemoradiotherapy (CRT) and consolidation chemotherapy. The specific regimen can vary, including options such as CapeOx (capecitabine and oxaliplatin), FOLFIRINOX (leucovorin, fluorouracil, irinotecan, and oxaliplatin), or 5-fluorouracil and leucovorin with or without oxaliplatin. The choice of regimen may depend on factors such as patient characteristics, tumor stage, and potential side effects.', 'The choice of initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is still a matter of debate. However, a recent study found that neoadjuvant mFOLFOXIRI chemotherapy improved pathological complete response rate, survival outcome, and reduced distant metastasis and anastomotic fistula rates compared to propensity-score matched controls of mFOLFOX6 neoadjuvant chemotherapy. This suggests that mFOLFOXIRI could be a more appropriate initial chemotherapy regimen in TNT for locally advanced rectal cancer patients. However, it is important to consider the higher incidence of grade III and/or IV nausea and/or vomiting associated with mFOLFOXIRI. Further studies are needed to confirm these findings and establish the optimum combination, sequence, or duration of TNT.', 'The initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is a combination of chemoradiotherapy, FOLFOX, and CAPOX.', 'The most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer patients is the modified FOLFOXIRI (mFOLFOXIRI), which has been demonstrated to improve pathological complete response rate and survival outcomes compared with propensity-score matched controls receiving mFOLFOX6 neoadjuvant chemotherapy. Additionally, mFOLFOXIRI reduces the rates of distant metastasis and anastomotic fistula.', 'The most appropriate initial chemotherapy regimen in total neoadjuvant therapy (TNT) for locally advanced rectal cancer patients is a combination of fluoropyrimidine-based chemotherapy, such as capecitabine or 5-fluorouracil (5-FU), with oxaliplatin (FOLFOX or CAPOX). This regimen has been shown to improve tumor response rates and increase the likelihood of achieving a complete pathological response. It is important to note that the choice of chemotherapy regimen may vary depending on individual patient factors and institutional protocols.', 'In Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer, the most appropriate initial chemotherapy regimen can vary based on specific patient factors and treatment goals. However, regimens like mFOLFOXIRI have shown promising results in improving the pathological complete response (pCR) rate and survival outcomes, as well as reducing the rate of distant metastasis and anastomotic fistula compared to mFOLFOX6. This makes mFOLFOXIRI a strong candidate for initial chemotherapy in TNT settings', 'The most appropriate initial chemotherapy regimen in Total Neoadjuvant Therapy (TNT) for locally advanced rectal cancer appears to be the neoadjuvant mFOLFOXIRI regimen. This regimen has shown to improve the pathological complete response (pCR) rate and survival outcomes, as well as reduce the rate of distant metastasis and anastomotic fistula compared to mFOLFOX6, according to studies with propensity-score matched controls.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37697712",
"http://www.ncbi.nlm.nih.gov/pubmed/34963563",
"http://www.ncbi.nlm.nih.gov/pubmed/30381141",
"http://www.ncbi.nlm.nih.gov/pubmed/37479897",
"http://www.ncbi.nlm.nih.gov/pubmed/37429749",
"http://www.ncbi.nlm.nih.gov/pubmed/37174033",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37174033",
"endSection": "abstract",
"offsetInBeginSection": 1243,
"offsetInEndSection": 1449,
"text": "A plethora of potential chemotherapy schedules are available around the radiotherapy component, which include ... | 13 | BioASQ-training13b | null | null | 65f7785dc4010b4d78000033 |
factoid | In what part of the cell would a SNARE Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) be found | ['membrane', 'nerve terminals', 'synaptic vesicles', 'endoplasmic reticulum (ER)', 'ERGIC', 'Golgi apparatus'] | ['SNARE soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are transmembrane proteins found in the endosomal/lysosomal system.', 'SNAREs are typically found in the membranes of cells where they play a crucial role in the process of membrane fusion.', 'SNAREs, including Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs), are found in the Golgi apparatus and endoplasmic reticulum of the cell.', 'Astrocytes, the most abundant glial cells in the central nervous system (CNS), sense synaptic activity and respond through the release of gliotransmitters, a process mediated by intracellular Ca. In these cells, SNARE Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are found on vesicles membranes and contribute to the docking and fusion of vesicles with the cell membrane, allowing the release of gliotransmitters to the extracellular space.', 'SNAREs are found in nerve terminals and synaptic vesicles.', 'Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (R-SNAREs) mainly promoted the assembly of the SNARE complex to drive the final membrane fusion step of membrane transport', 'A SNARE Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) would be found in presynaptic terminals and perisynaptic astrocytic processes.', 'Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) can be found in various parts of the cell, including the plasma membrane, endoplasmic reticulum, Golgi apparatus, and synaptic vesicles. They are involved in mediating membrane fusion and play a crucial role in intracellular vesicle trafficking, neurotransmitter release, and other cellular processes.', "SNARE proteins are located in the cell's membranes, including those of synaptic vesicles and the plasma membrane.", 'Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) would be found in secretory vesicles.', 'SNAREs are found in the trans-Golgi network.', 'SNAREs are found in the plasma membrane and vesicles.', '\nSNAREs are transmembrane proteins found in various organelles and vesicles involved in vesicle trafficking and secretion, such as synaptic vesicles, endoplasmic reticulum (ER), Golgi apparatus, and lysosomes. In synapses, SNAREs are located in both presynaptic and postsynaptic membranes.', 'SNAREs are found in the plasma membrane of the cell, where they play a crucial role in membrane fusion and transport.', 'Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are found in the membrane.', 'The SNARE Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are found in the cell membrane.', 'SNARE proteins are primarily found in the cytoplasm of cells, where they play a crucial role in membrane fusion and intracellular transport processes.', 'SNAREs are found in the plasma membrane of neuronal presynaptic terminals.', 'SNAREs are found in the cell membrane.', 'Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) would be found in nerve terminals, synaptic vesicles, and in nerve terminals.', 'SNARE proteins are primarily found in nerve terminals, synaptic vesicles, endosomes, and the astrocytic plasma membrane.', 'SNAREs (Soluble N-ethylmaleimide-sensitive factor attachment protein receptors) are specialized proteins, involved in the process of vesicle fusion in a cell. They are typically located in the plasma membrane and vesicle membrane.', 'SNAREs are found in the plasma membrane of cells.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36750663",
"http://www.ncbi.nlm.nih.gov/pubmed/11427709",
"http://www.ncbi.nlm.nih.gov/pubmed/19617396",
"http://www.ncbi.nlm.nih.gov/pubmed/20589833",
"http://www.ncbi.nlm.nih.gov/pubmed/12517971",
"http://www.ncbi.nlm.nih.gov/pubmed/16536742",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37465385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (R-SNAREs) mainly promoted the assembly of ... | 13 | BioASQ-training13b | null | null | 66088d66fdcbea915f00000c |
factoid | What disease is treated with Teplizumab? | ['type 1 diabetes'] | ['Teplizumab is a CD3-directed monoclonal antibody that was approved for type 1 diabetes (T1D) and was shown to delay the onset of Stage 3 T1D in adults and pediatric patients 8 years of age and older with Stage 2 T1D, based on results of a clinical trial in high-risk relatives of individuals with T1D.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/34936848",
"http://www.ncbi.nlm.nih.gov/pubmed/37296593",
"http://www.ncbi.nlm.nih.gov/pubmed/35533645",
"http://www.ncbi.nlm.nih.gov/pubmed/37004543",
"http://www.ncbi.nlm.nih.gov/pubmed/37607392",
"http://www.ncbi.nlm.nih.gov/pubmed/36877454",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37502867",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Teplizumab has been approved for the delay of the onset of type 1 diabetes and may modulate new onset disease."
... | 13 | BioASQ-training13b | null | null | 65cf6ae91930410b13000007 |
factoid | What is the target of Divarasib? | ['KRAS G12C'] | ['Divarasib is a KRAS G12C inhibitor.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37611121",
"http://www.ncbi.nlm.nih.gov/pubmed/37774359",
"http://www.ncbi.nlm.nih.gov/pubmed/38052910"
] | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37611121",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Single-Agent Divarasib (GDC-6036) in Solid Tumors with a KRAS G12C Mutation."
},
{
"beginSection": "abstract",
... | 13 | BioASQ-training13b | null | null | 65cfaf7e1930410b13000016 |
factoid | What is the appropriate treatment in HER2Neu amplificated refractory advanced colorectal cancer patients? | ['Tucatinib plus trastuzumab'] | ['1) HER2Neu amplification occurs in approximately 2-5% of colorectal cancer patients. 2) Chemotherapy with standard agents such as oxaliplatin or irinotecan and fluoropyrimidines remains the first-line treatment in HER2Neu amplified refractory advanced colorectal cancer. 3) Trastuzumab, an anti-HER2Neu monoclonal antibody, has shown promising results in combination with standard chemotherapy in patients with HER2Neu amplified metastatic colorectal cancer.', 'The most appropriate treatment in HER2Neu amplificated refractory advanced colorectal cancer patients is tucatinib plus trastuzumab.', 'The appropriate treatment for HER2Neu amplified refractory advanced colorectal cancer patients would be regorafenib plus PD-1 inhibitor therapy, as this combination has shown promising efficacy in a real-world study. Patients with ERBB2/ERBB3 mutation may be the preferred population for this combination regimen.', 'Tucatinib plus trastuzumab had clinically meaningful anti-tumour activity and favourable tolerability. This treatment is the first US Food and Drug Administration-approved anti-HER2 regimen for metastatic colorectal cancer and is an important new treatment option for chemotherapy-refractory HER2-positive metastatic colorectal cancer.', 'Currently, the optimal treatment in HER2Neu amplificated refractory advanced colorectal cancer patients is not well established. Targeted therapy for patients with HER2/neu amplification in refractory mCRC is still being evaluated. HER2/neu amplification occurs in a minority of patients with refractory mCRC (2-6%), and data on treatment of HER2/neu amplified mCRC is still limited. However, several studies are underway to evaluate the role of anti-HER2/neu agents (trastuzumab or trastuzumab deruxtecan) in this subgroup.', 'The appropriate treatment for HER2Neu amplificated refractory advanced colorectal cancer patients is tucatinib (a small molecule HER2 inhibitor) in combination with trastuzumab (a monoclonal antibody against HER2). This treatment was recently approved by the US Food and Drug Administration for this specific patient population who have previously received chemotherapy. This is the first approved anti-HER2 regimen for metastatic colorectal cancer.', 'The appropriate treatment for HER2-positive, metastatic colorectal cancer patients who have not responded to chemotherapy is Tucatinib plus trastuzumab, which is the first US Food and Drug Administration-approved anti-HER2 regimen for this condition.', 'The appropriate treatment for HER2Neu amplified, chemotherapy-refractory advanced colorectal cancer patients is the combination of tucatinib plus trastuzumab. This regimen has demonstrated clinically meaningful anti-tumor activity and favorable tolerability in this patient population. It is the first US Food and Drug Administration-approved anti-HER2 regimen for metastatic colorectal cancer, making it an important new treatment option for these patients.', 'Tucatinib plus trastuzumab had clinically meaningful anti-tumour activity and favourable tolerability, making it the appropriate treatment in HER2Neu amplificated refractory advanced colorectal cancer patients.', 'HER2 amplification and/or activating mutations are present in 4% of metastatic colorectal cancers. To date, there are no approved therapies for HER2-positive metastatic colorectal cancer. Tucatinib plus trastuzumab is the first US Food and Drug Administration-approved anti-HER2 regimen for metastatic colorectal cancer.', 'For patients with HER2-amplified metastatic colorectal cancer refractory to standard treatment, anti-HER2 targeted therapies have shown promising activity. Potential treatment options include:\n\n- Dual HER2-targeted therapy with trastuzumab plus pertuzumab\n- Trastuzumab deruxtecan \n- Combination of trastuzumab and lapatinib\n- Pyrotinib (for patients resistant to trastuzumab and lapatinib)\n\nRecent evidence suggests anti-HER2 strategies could potentially represent a new standard of care in this patient population. However, secondary resistance to HER2-targeted agents can occur in most cases.', 'Tucatinib plus trastuzumab has shown clinically meaningful anti-tumour activity and favorable tolerability in patients with HER2-positive metastatic colorectal cancer refractory to chemotherapy. This treatment regimen is the first FDA-approved anti-HER2 therapy for metastatic colorectal cancer, providing an important new treatment option for patients with this condition.', 'Trastuzumab deruxtecan showed promising and durable activity in HER2-positive metastatic colorectal cancer refractory to standard treatment, with a safety profile consistent with that reported in previous trastuzumab deruxtecan trials.', 'The appropriate treatment for HER2Neu amplified refractory advanced colorectal cancer (mCRC) remains an area of active research and debate. While the HERACLES trial did not meet its primary endpoint of objective response rate, the combination of pertuzumab and trastuzumab deruxtecan demonstrated promising disease control rates and progression-free survival in this patient population. Additionally, a real-world study found that regorafenib plus PD-1 inhibitor therapy was effective in refractory microsatellite stable mCRC with ERBB2/ERBB3 mutation. However, there is currently no standard of care for HER2Neu amplified refractory advanced colorectal cancer patients. Clinical trials are ongoing to further evaluate the safety and efficacy of these and other treatment regimens in this population.', 'The appropriate treatment in HER2Neu amplified refractory advanced colorectal cancer patients includes the use of neratinib, trastuzumab deruxtecan, and trastuzumab.', 'HER2Neu amplification is a molecular alteration that can lead to resistance to anti-EGFR monoclonal antibodies (mAbs) in colorectal cancer (CRC). Recent evidence suggests that anti-ERBB2 therapeutic strategies, such as trastuzumab deruxtecan, are active in patients with ERBB2-positive metastatic CRC and could potentially represent a new standard-of-care. Pyrotinib is a promising new candidate for salvage therapy in patients with HER2-positive metastatic CRC who have developed resistance to trastuzumab and lapatinib. Dual HER2-targeted therapy with pertuzumab plus trastuzumab is also an option for patients with heavily pretreated, HER2-amplified metastatic CRC. Rechallenge with anti-EGFR inhibitors, in case of persistent or recovery of RAS-wildness, and targeted approach of specific mutations (BRAF inhibitors), amplifications (anti-Her2 treatment), or fusion proteins (NTRK inhibitors) can be guided by the use of next-generation sequencing (NGS).', "The appropriate treatment for HER2-positive refractory advanced colorectal cancer patients is the combination of tucatinib and trastuzumab. This regimen has shown clinically meaningful anti-tumor activity and is well-tolerated. It's also the first FDA-approved anti-HER2 therapy specifically for metastatic colorectal cancer, making it a significant new option for patients who have not responded to chemotherapy.", 'The recommended treatment for HER2Neu amplificated refractory advanced colorectal cancer patients is Tucatinib plus trastuzumab.', 'Tucatinib plus trastuzumab is the appropriate treatment in HER2Neu amplificated refractory advanced colorectal cancer patients.', 'The appropriate treatment in HER2Neu amplificated refractory advanced colorectal cancer patients is the combination of pyrotinib and trastuzumab.', "The study suggests that tucatinib plus trastuzumab has clinically meaningful anti-tumor activity and favorable tolerability in patients with HER2Neu amplificated refractory advanced colorectal cancer. This treatment is the first US Food and Drug Administration-approved anti-HER2 regimen for metastatic colorectal cancer and is an important new treatment option for chemotherapy-refractory HER2-positive metastatic colorectal cancer. Therefore, it would be appropriate to consider tucatinib plus trastuzumab as a treatment option for these patients. However, it is essential to consider each patient's individual circumstances and potential risks and benefits when making treatment decisions.", 'For patients with advanced colorectal cancer and HER2Neu amplification who have not responded to prior treatments, recommended therapies include tucatinib plus trastuzumab, trastuzumab deruxtecan, pyrotinib and trastuzumab, or neratinib combined with cetuximab.', 'The appropriate treatment in HER2Neu amplificated refractory advanced colorectal cancer patients is the combination of trastuzumab and lapatinib.', 'For patients with HER2Neu amplified refractory advanced colorectal cancer, the combination of Tucatinib and Trastuzumab is a clinically meaningful and FDA-approved treatment option.', 'The appropriate treatment for HER2-positive refractory advanced colorectal cancer patients is tucatinib plus trastuzumab. This regimen has shown clinically meaningful anti-tumor activity and favorable tolerability.', 'The appropriate treatment for HER2Neu amplified refractory advanced colorectal cancer patients is trastuzumab (Herceptin).', 'The recommended treatments for HER2Neu amplificated refractory advanced colorectal cancer patients are trastuzumab deruxtecan, neratinib, and tucatinib plus trastuzumab.', 'Tucatinib plus trastuzumab has clinically meaningful anti-tumour activity and favourable tolerability in HER2Neu amplificated refractory advanced colorectal cancer patients. This treatment is the first US Food and Drug Administration-approved anti-HER2 regimen for metastatic colorectal cancer and is an important new treatment option for chemotherapy-refractory HER2-positive metastatic colorectal cancer.', 'The appropriate treatment in HER2Neu amplificated refractory advanced colorectal cancer patients is the combination of tucatinib and trastuzumab. This treatment has shown clinically meaningful anti-tumor activity and favorable tolerability, making it the first FDA-approved anti-HER2 regimen for metastatic colorectal cancer. It is an important new treatment option for patients with chemotherapy-refractory HER2-positive metastatic colorectal cancer.', 'Tucatinib plus trastuzumab had clinically meaningful anti-tumour activity and favourable tolerability', 'It is currently assumed that patients who have received standard chemotherapy and have no evidence of recurrent disease should be treated with targeted therapy alone. In particular, HER2-positive patients who have received chemotherapy and have a good performance status should be treated with a combination of targeted therapy and chemotherapy.', '-In HER2Neu amplificated refractory advanced colorectal cancer patients, anti-HER2 therapies have shown promising activity. \n-Anti-HER2 therapies include trastuzumab and lapatinib, and these should be considered as potential therapeutic options in this specific patient population. \n-Currently, there are no formal recommendations for the use of anti-HER2 therapies in refractory colorectal cancer, and further studies are needed to establish the optimal treatment approach.', 'The FDA approved combination of trastuzumab and pertuzumab for use in metastatic breast cancer has shown promising results in HER2-positive refractory advanced colorectal cancer patients, with an objective response rate (ORR) of 38% and a disease control rate (DCR) of 76.9%. This treatment regimen is currently being evaluated for its safety and efficacy in larger clinical trials, making it a potential new option for patients with HER2-positive metastatic colorectal cancer who have progressed on standard chemotherapy regimens.', "The appropriate treatment for HER2-positive refractory advanced colorectal cancer patients is the combination of tucatinib and trastuzumab. This regimen has shown clinically meaningful anti-tumor activity and is well-tolerated. It's significant as it's the first FDA-approved anti-HER2 therapy for metastatic colorectal cancer, offering a new treatment option for those with chemotherapy-refractory disease.", ' The appropriate treatment for advanced coloreCTal cancer with H ER-pos and SCFV translocation is a multidrug approach involving the use of monoclonal antibodies, antibody-drug conjugates, and immune checkpoint inhibitors. ideal_answer: The appropriate treatment for advanced coloreCTal cancer with H ER-pos and SCFV translocation is a multidrug approach involving the use of monoclonal antibodies, antibody-drug conjugates, and immune checkpoint inhibitors. This approach combines the targeted elimination of cancer cells with the activation of the immune system to recognize and eliminate tumor cells. ', 'The appropriate treatment for HER2Neu amplificated refractory advanced colorectal cancer patients is the combination of tucatinib and trastuzumab. This treatment has shown clinically meaningful anti-tumour activity and favorable tolerability. It is the first FDA-approved anti-HER2 regimen for metastatic colorectal cancer and provides an important new treatment option for patients who have not responded to chemotherapy.', 'In HER2neu amplificated refractory advanced colorectal cancer patients, the appropriate treatment option is the combination of HER2-targeted therapy with chemotherapy. This can include the use of trastuzumab, a monoclonal antibody targeting HER2, in combination with chemotherapy agents such as 5-fluorouracil (5-FU) or oxaliplatin. The addition of trastuzumab to chemotherapy has shown improved outcomes in HER2-positive colorectal cancer patients, including increased response rates and prolonged survival. However, further studies are needed to determine the optimal treatment regimen and the role of other HER2-targeted agents in this patient population.', 'The appropriate treatment for HER2Neu amplified refractory advanced colorectal cancer patients may include combination targeted therapy with agents such as trastuzumab and lapatinib, which have shown activity in other HER2-positive malignancies. Additionally, enrollment in clinical trials exploring novel HER2-targeted therapies or combinatorial strategies could offer potential benefits for these patients who are resistant to standard treatments.', 'Tucatinib plus trastuzumab is an appropriate treatment option for HER2-positive metastatic colorectal cancer patients who are refractory to chemotherapy.', 'In HER2Neu amplified refractory advanced colorectal cancer patients, appropriate treatments may include targeted therapies such as trastuzumab deruxtecan, dual HER2-targeted therapy with pertuzumab plus trastuzumab, or the combination of trastuzumab and lapatinib. These treatments have shown promising activity and tolerability in patients with HER2-positive metastatic colorectal cancer who have developed resistance to standard therapies. Additionally, novel targeted treatments under development, such as anti-ERBB2 therapeutic strategies, may also be considered as potential options for these patients.', 'Tucatinib plus trastuzumab is the first US Food and Drug Administration-approved anti-HER2 regimen for metastatic colorectal cancer and is an important new treatment option for chemotherapy-refractory HER2-positive metastatic colorectal cancer.', 'Trastuzumab plus erlotinib is the standard of care for HER2-amplified, treatment-refractory metastatic colorectal cancer.', 'The appropriate treatment for HER2Neu amplified refractory advanced colorectal cancer patients is a combination of tucatinib and trastuzumab. This regimen has shown clinically meaningful anti-tumor activity and is well-tolerated, making it a significant new option for patients whose cancer has not responded to chemotherapy', 'Cetuximab plus bevacizumab is an effective treatment for HER2Neu amplified refractory advanced colorectal cancer patients.', 'The new treatment option for refractory HER2-positive metastatic colorectal cancer is Tucatinib plus trastuzumab. It is a US Food and Drug Administration-approved anti-HER2 regimen for metastatic colorectal cancer.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33005299",
"http://www.ncbi.nlm.nih.gov/pubmed/35228040",
"http://www.ncbi.nlm.nih.gov/pubmed/36550683",
"http://www.ncbi.nlm.nih.gov/pubmed/35238866",
"http://www.ncbi.nlm.nih.gov/pubmed/33961795",
"http://www.ncbi.nlm.nih.gov/pubmed/35649212",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37142372",
"endSection": "abstract",
"offsetInBeginSection": 3128,
"offsetInEndSection": 3463,
"text": "Tucatinib plus trastuzumab had clinically meaningful anti-tumour activity and favourable tolerability. This tr... | 13 | BioASQ-training13b | null | null | 65f77a71c4010b4d7800003b |
factoid | What type of drug is administered to the mother for the prevention of lung immaturity when a preterm delivery is anticipated? | ['Corticosteroids'] | ['Corticosteroids are the drug administered to the mother for the prevention of lung immaturity when a preterm delivery is anticipated.', 'Corticosteroids administered to the mother accelerate development of immature lung in premature babies intra utero.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33423644",
"http://www.ncbi.nlm.nih.gov/pubmed/35943347",
"http://www.ncbi.nlm.nih.gov/pubmed/33368142"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33423644",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 388,
"text": "The administration of antenatal corticosteroids, in cases of imminent preterm delivery, can enhance fetal lung m... | 13 | BioASQ-training13b | null | null | 660bb7f9fdcbea915f000029 |
factoid | What is the most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients? | ['1650 mg/m2', '1650 m(2)', '825 mg/m(2) twice-daily'] | ['The most appropriate dose of capecitabine for concurrent treatment with radiotherapy in neoadjuvant therapy of locally advanced rectal cancer patients is generally considered to be 1650 mg/m² per day, as this dosage has been used effectively in clinical trials and aligns with current guidelines.', 'capecitabine was administered daily at a dose of 1650 mg/m(2) during the entire course of radiation therapy.', 'The optimal dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer has been studied, and various doses have been used in clinical trials. However, there is no definitive consensus on the ideal dose due to differences in study designs, patient populations, and treatment regimens. In some studies, capecitabine was administered at a dose of 800 mg/m² orally twice daily during radiotherapy, while others have used doses ranging from 625 to 1,250 mg/m² per day. The choice of dose should be based on the balance between efficacy and toxicity, as well as individual patient factors such as performance status, comorbidities, and tolerance to treatment. Clinical judgment and guidelines from expert panels can provide guidance in selecting an appropriate capecitabine dose for each patient undergoing neoadjuvant chemoradiotherapy for rectal cancer.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is typically around 825 mg/m² twice daily. This dose has been commonly used in various studies in combination with radiotherapy and other chemotherapy agents like oxaliplatin or irinotecan. The specific dosing regimen may vary slightly depending on the study protocol, but the dose range of capecitabine used in these treatments is generally consistent around 825 mg/m² twice daily.', 'In the study mentioned, the most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients was 1650 mg/m(2) administered daily during the entire course of radiation therapy.', 'The most appropriate dose of capecitabine when used concurrently with radiotherapy for neoadjuvant therapy in patients with locally advanced rectal cancer is 1650 mg/m² daily throughout the entire course of radiation therapy', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 1650 mg/m(2).', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 825 mg/m2 twice-daily. This dose is recommended in multiple studies and has been shown to be effective and well-tolerated in combination with radiotherapy and other chemotherapy agents.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 1,600 mg/m2.', 'Based on the study, the most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer is 1650 mg/m2 daily during the entire course of radiation therapy. This dosage was used in a prospective Phase II trial and was found to have low toxicity while achieving encouraging rates of tumor downstaging and sphincter preservation. However, further studies may be needed to confirm these findings and establish this dose as the standard.', 'The most appropriate dose of capecitabine for concurrent treatment with radiotherapy in neoadjuvant therapy of locally advanced rectal cancer patients is 1650 mg/m² daily. This dosage is administered throughout the entire course of radiation therapy.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 1650 mg/m(2) daily.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 1650 mg/m(2) administered daily during the entire course of radiation therapy.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients has been studied in clinical trials. A phase I trial evaluated the safety and efficacy of capecitabine given twice daily during pelvic irradiation in patients with resectable rectal cancer. The maximum tolerated dose (MTD) was reached at a dose level of 2000 mg m(-2) day(-1), but dose escalation was ceased at 1800 mg m(-2) day(-1) after reaching MTD. A phase II trial evaluated the feasibility and efficacy of concurrent radiotherapy and capecitabine in rectal cancer patients. The recommended dose for further evaluation was established at capecitabine 825 mg/m(2) bid, administered without break during a conventional radiotherapy period of about ', 'The most appropriate dose of capecitabine for concurrent use with radiation in neoadjuvant therapy for locally advanced rectal cancer is 1650 mg/m(2) daily.', 'Capecitabine was administered daily at a dose of 1650 mg/m(2) during the entire course of radiation therapy.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients has not been definitively established. The standard dose of capecitabine used in clinical practice is 1650 mg/m(2) per day, which is the dose used in the landmark phase III trial that demonstrated the efficacy and safety of capecitabine in this setting. However, some studies have suggested that a lower dose of capecitabine (e.g., 1250 mg/m(2) per day) may be equally effective and less toxic. The choice of dose should be individualized based on patient factors, such as age, performance status, and comorbidities, as well as the radiation dose and fractionation scheme used.', 'The most appropriate dose of capecitabine for concurrent treatment with radiotherapy in neoadjuvant therapy of locally advanced rectal cancer patients is 1650 mg/m(2) daily.', 'capecitabine was administered daily at a dose of 1650 mg/m(2) during the entire course of radiation therapy', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 1650 mg/m(2) daily for 14 days.', 'Based on the information provided, capecitabine was administered daily at a dose of 1650 mg/m(2) during the entire course of radiation therapy for neoadjuvant treatment of locally advanced rectal cancer patients.', 'The appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients has not been definitively established. However, a phase I trial of capecitabine and weekly irinotecan in combination with radiotherapy for neoadjuvant therapy of rectal cancer found that the maximum tolerated dose (MTD) of capecitabine was 625 mg/m(2) bid, given concurrently with weekly irinotecan and pelvic radiotherapy. The MTD was determined based on the incidence of dose-limiting toxicities, primarily diarrhea. However, larger phase II trials are needed to confirm the efficacy and safety of this dose and schedule.', 'Based on the information provided, the most commonly used dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 825 mg/m2 twice daily, administered continuously or on days 1-14 and 22-35 of radiotherapy. Some key findings:\n\n- Capecitabine 825 mg/m2 twice daily for 7 days/week was found to be an effective and tolerable continuous dosing regimen. \n- Capecitabine 825 mg/m2 twice daily on days 1-14 and 22-35 was used in combination with oxaliplatin and radiotherapy in one study.\n- Several studies used capecitabine at 825 mg/m2 twice daily concomitantly with radiotherapy.\n\nWhile some variations in dosing schedules exist, capecitabine 825 mg/m2 twice daily, either continuously or on select days concurrent with radiotherapy, appears to be a standard neoadjuvant regimen for locally advanced rectal cancer based on the provided abstracts.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 1650 mg/m2 daily during the entire course of radiation therapy.', '1650 mg/m(2) of capecitabine is the most appropriate dose for concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients.', 'Capecitabine was administered orally at a dose of 825 mg/m(2) twice-daily concomitantly every day during pelvic irradiation.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 1650 mg/m² per day, administered orally during the entire course of radiation therapy. This dose has been shown to improve pathological complete response rates and decrease local recurrence rates in clinical trials. However, the specific dose and duration of capecitabine and radiotherapy may vary based on individual patient factors and the discretion of the treating healthcare provider. It is always recommended to consult with a healthcare professional for personalized treatment recommendations.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 825 mg/m^2^ bid, administered without break during a conventional radiotherapy period of about 6 weeks. This dosage was determined based on the results of a phase I trial that established the feasibility of concurrent radiotherapy and capecitabine and defined the maximum-tolerated dose (MTD) in patients with rectal cancer. The recommended dose for further evaluation is capecitabine 825 mg/m^2^ bid, which showed acceptable toxicity and promising response rates in preoperative chemoradiation based on RT at 45 Gy in 25 daily fractions over 5 weeks with continuous daily oral capecitabine at 650 mg m^2^ b.i.d. days 1-35 and weekly IV irinotecan at', 'Preoperative concomitant radiation therapy with oral capecitabine for locally advanced rectal cancer is feasible and safe. It is well tolerated. The most suitable dose of capecitabine is 825 mg/m2 twice daily every day during the entire course of radiation therapy.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 825 mg/m² delivered orally twice daily for the duration of radiotherapy.', 'The most appropriate dose of capecitabine for concurrent treatment with radiotherapy in neoadjuvant therapy of locally advanced rectal cancer patients is 1650 mg/m(2) daily during the entire course of radiation therapy.', '825 mg/m2, twice daily, administered continuously, during radiotherapy, and until 1 week after the last fraction of radiotherapy.', '1650 mg/m(2) daily during the entire course of radiation therapy.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 1650 mg/m² administered daily throughout the course of radiation therapy.', '1650 mg/m(2)', '1650 mg/m(2) is the most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 1250 mg/m2 per day for 2 weeks followed by 5-fluorouracil (5-FU) 400 mg/m2 per day for 5 days, with a total of 6 cycles.', '825 mg/m^2^ twice daily on days 1-38 of chemoradiotherapy for neoadjuvant treatment of locally advanced rectal cancer patients.', 'The most suitable dose of capecitabine for concurrent use with radiotherapy in neoadjuvant therapy for locally advanced rectal cancer is either 825 mg/m(2) twice daily or 900 mg/m(2) twice daily, depending on the specific trial and patient tolerance.', '825 mg/m² twice daily during radiotherapy and at weekends is considered the most appropriate dose of capecitabine for concurrent treatment in neoadjuvant therapy of locally advanced rectal cancer patients.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 825 mg/m2 twice daily, given on the days of radiotherapy, with a maximum daily dose of 1650 mg/m2.', 'The recommended dose for phase II evaluation is capecitabine 825 mg/m(2) bid, administered without break during a conventional radiotherapy period of about 6 weeks.', 'The most appropriate dose of capecitabine in concurrent treatment with radiotherapy for neoadjuvant therapy of locally advanced rectal cancer patients is 825 mg.', '\nAnswer: 825 mg/m² twice daily on days 1-14 of radiotherapy, as recommended by the National Comprehensive Cancer Network (NCCN) guidelines for colorectal cancer. Alternatively, daily 1600 mg/m² (2 cycles, separated by a 7-day rest) as determined in a phase I study. Consult with a healthcare provider for personalized treatment recommendations.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/17987042",
"http://www.ncbi.nlm.nih.gov/pubmed/22855196",
"http://www.ncbi.nlm.nih.gov/pubmed/25102935",
"http://www.ncbi.nlm.nih.gov/pubmed/19508705",
"http://www.ncbi.nlm.nih.gov/pubmed/17385825",
"http://www.ncbi.nlm.nih.gov/pubmed/12243814",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15913913",
"endSection": "abstract",
"offsetInBeginSection": 587,
"offsetInEndSection": 694,
"text": "capecitabine was administered daily at a dose of 1650 mg/m(2) during the entire course of radiation therapy"
}... | 13 | BioASQ-training13b | null | null | 66099c01fdcbea915f000023 |
factoid | What part of the cell is mitophagy associated with? | ['mitochondria'] | ['Mitophagy is a specific type of autophagy that involves the selective elimination of damaged or dysfunctional mitochondria via autophagosomes and lysosomes, a process that is critical for mitochondrial quality control.', 'Mitophagy is associated with the mitochondria, which are critical cellular energy resources and central to the life of the neuron. Mitophagy selectively clears damaged or dysfunctional mitochondria through autophagic machinery to maintain mitochondrial quality control and homeostasis.', 'Mitophagy is a selective form of autophagy, where damaged or dysfunctional mitochondria are targeted and degraded by the autophagosome.', 'Mitophagy is associated with mitochondria.', 'Mitophagy is associated with mitochondria, involving their encapsulation into autophagosomes for delivery to lysosomes for degradation.', 'Mitophagy is associated with "mitochondria".', ' Mitophory are primarily associated with the organelle membrane of eukaryotes, where they play a crucial role in the degradation of misfolded proteins and the maintenance of cellular integrity. ', 'Mitophagy is associated with mitochondria, the part of the cell responsible for energy production. It specifically targets damaged or dysfunctional mitochondria for degradation to maintain cellular health', 'Mitophagy is a selective autophagy of mitochondria, can efficiently degrade, remove and recycle the malfunctioning or damaged mitochondria, and is crucial for quality control.', 'Mitophagy, or selective autophagy of mitochondria, is an essential pathway to preserve mitochondrial homeostasis by clearing up damaged mitochondria', 'Mitophagy is associated with the lysosomes, which are responsible for the degradation of damaged or superfluous mitochondria.', 'Mitophagy is associated with the mitochondria, which are the powerhouses of the cell.', 'Mitophagy is a process by which cells selectively remove and burn their own mitochondria. It is a conserved mechanism that all eukaryotes use to remove damaged mitochondria.', 'Mitophagy is associated with the clearance of damaged mitochondria via lysosomes.', 'Mitophagy is associated with mitochondria. It is the selective autophagy of damaged or dysfunctional mitochondria to maintain mitochondrial homeostasis and quality control.', 'Mitophagy is a selective form of autophagy that specifically targets damaged or dysfunctional mitochondria for degradation and recycling. It is a quality control mechanism associated with maintaining a healthy mitochondrial pool within the cell.', 'Mitophagy is associated with mitochondria, which are organelles within eukaryotic cells. Mitophagy is a process by which cells selectively remove and recycle damaged or dysfunctional mitochondria through the autophagy-lysosome pathway. This helps to maintain mitochondrial quality control and homeostasis.', 'Mitophagy is an essential physiological process that eliminates damaged mitochondria via lysosomes.', 'Mitophagy is associated with the outer mitochondrial membrane 20 (Tomm20), a mitochondrial translocase that, when ubiquitinated, promotes mitophagy.', 'Mitophagy is an essential pathway responsible for preserving mitochondrial homeostasis through the clearance of damaged mitochondria.', 'Mitophagy refers to selective autophagy of mitochondria, which plays a crucial role in preserving mitochondrial homeostasis by clearing up damaged or dysfunctional mitochondria.', 'Mitophagy is associated with the mitochondria, targeting them for degradation.', 'Mitophagy is associated with the elimination of damaged mitochondria and maintenance of mitochondrial homeostasis. It is a process that occurs within the cell, specifically targeting and removing dysfunctional or damaged mitochondria.', 'Mitophagy is associated with the selective autophagic clearance of flawed or damaged mitochondria within the cell, ensuring the maintenance of a healthy mitochondrial pool and cellular homeostasis.', 'Mitochondrial autophagy is associated with the removal of defective mitochondria from the cell by internalisation into autophagosomes which fuse with lysosomes.', 'Mitophagy is associated with mitochondria, the part of the cell responsible for energy production. It specifically targets damaged or dysfunctional mitochondria, clearing them out to maintain cellular health and efficiency.', 'Mitophagy is associated with the process of selectively clearing damaged or dysfunctional mitochondria through autophagic machinery to maintain mitochondrial quality control and homeostasis within the cell.', 'Mitophagy is associated with lysosomes, where defective mitochondria are internalized into autophagosomes that fuse with lysosomes for degradation.', "Mitophagy is a process associated with the elimination of damaged or dysfunctional mitochondria through autophagic machinery, which is a part of the cell's quality control and homeostasis maintenance mechanism.", 'Mitophagy is associated with mitochondria, which are organelles within eukaryotic cells. Mitophagy is a process by which cells selectively remove and recycle damaged or dysfunctional mitochondria through the autophagy-lysosome pathway. This process helps to maintain mitochondrial quality control and homeostasis.', 'Mitophagy is associated with the mitochondria.', 'Mitophagy is associated with mitochondria, specifically targeting damaged or dysfunctional mitochondria for degradation to maintain cellular health.', 'Mitophagy is associated with the lysosomes, which are responsible for the degradation of damaged or dysfunctional mitochondria.', 'Mitophagy is associated with mitochondria through autophagic machinery to maintain mitochondrial quality control and homeostasis.', 'Mitophagy is associated with lysosomes.', 'Mitophagy is associated with the outer membrane of mitochondria (OMM).', 'Mitochondrial dysfunction is targeted for degradation in the lysosomes by mitophagy.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25753537",
"http://www.ncbi.nlm.nih.gov/pubmed/29311991",
"http://www.ncbi.nlm.nih.gov/pubmed/37488884",
"http://www.ncbi.nlm.nih.gov/pubmed/25634658",
"http://www.ncbi.nlm.nih.gov/pubmed/36740450",
"http://www.ncbi.nlm.nih.gov/pubmed/32131138",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37488884",
"endSection": "abstract",
"offsetInBeginSection": 360,
"offsetInEndSection": 510,
"text": "Mitophagy, or selective autophagy of mitochondria, is an essential pathway to preserve mitochondrial homeostasis... | 13 | BioASQ-training13b | null | null | 660877c8fdcbea915f000008 |
factoid | What channel is targeted by VX-548? | ['NaV1.8'] | ['VX-548 is an oral, highly selective inhibitor of NaV1.8 that is studied for control of acute pain.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37530822"
] | [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37530822",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 58,
"text": "Selective Inhibition of NaV1.8 with VX-548 for Acute Pain."
},
{
"beginSection": "abstract",
"document": "htt... | 13 | BioASQ-training13b | null | null | 65cfd02e1930410b1300001c |
factoid | What is the most effective drug for oxaliplatin-induced neuropathy? | ['Duloxetine'] | ['There are several drugs that have been studied for their potential in treating oxaliplatin-induced neuropathy, including pregabalin, duloxetine, oxycodone, and riluzole. However, the most effective drug for oxaliplatin-induced neuropathy is still unknown, as different studies have shown varying results. A systematic review and meta-analysis of available studies would be necessary to determine the most effective drug for this condition.', 'The most effective drugs for treating oxaliplatin-induced neuropathy include pregabalin, duloxetine, and oxycodone, with mexiletine, omeprazole, and Calmangafodipir also showing effectiveness.', 'Duloxetine, a serotonin and norepinephrine reuptake inhibitor, is the best-established treatment for painful chemotherapy-induced peripheral neuropathy (CIPN). Despite intense investigation at the preclinical and clinical levels, no treatment can be suggested for the prevention of Oxaliplatin-induced peripheral neurotoxicity (OIPN), and only limited evidence for the efficacy of duloxetine in the treatment setting has been provided.', "The most effective drugs for treating oxaliplatin-induced neuropathy are those that target specific mechanisms of nerve damage and pain perception, such as gabapentinoids (like gabapentin or pregabalin), which work by inhibiting voltage-dependent calcium channels to reduce the release of neurotransmitters involved in pain signaling. Other medications used include duloxetine, a serotonin-norepinephrine reuptake inhibitor that has been shown to be effective for managing chemotherapy-induced neuropathic pain. Additionally, tricyclic antidepressants like amitriptyline and selective serotonin reuptake inhibitors (SSRIs) can also be used off-label for their analgesic effects in treating neuropathy. It is important to note that the choice of medication should be individualized based on a patient's specific symptoms, overall health status, and potential drug interactions.", 'There is currently no single "most effective" drug for oxaliplatin-induced neuropathy, as treatment options are often individualized based on the severity of symptoms and patient preferences. However, duloxetine and pregabalin are commonly used medications for managing neuropathic pain associated with oxaliplatin-induced neuropathy. Other treatments may include tricyclic antidepressants, opioids, or topical agents. Additionally, there is ongoing research into potential neuroprotective agents that may prevent or reduce the severity of oxaliplatin-induced neuropathy.', 'The most effective drug for oxaliplatin-induced neuropathy is duloxetine, a serotonin and norepinephrine reuptake inhibitor. Duloxetine has been shown to be the best-established treatment for painful chemotherapy-induced peripheral neuropathy (CIPN).', 'Duloxetine is the most effective drug for oxaliplatin-induced neuropathy, according to a systematic review and meta-analysis published in the Journal of Clinical Oncology in 2019. The review analyzed data from 11 randomized controlled trials involving 1,225 patients with chemotherapy-induced peripheral neuropathy (CIPN) caused by oxaliplatin. The study found that duloxetine significantly reduced the severity and incidence of CIPN compared to placebo or standard care. Other drugs that have shown some effectiveness in managing oxaliplatin-induced neuropathy include gabapentin, pregabalin, and amitriptyline, but duloxetine appears to be the most effective.', 'Amifostine is the most effective drug for oxaliplatin-induced neuropathy.', 'Duloxetine is the most effective drug for oxaliplatin-induced neuropathy, according to a systematic review and meta-analysis published in the Journal of Clinical Oncology in 2019. The review analyzed data from 11 randomized controlled trials involving 1,212 patients with chemotherapy-induced peripheral neuropathy (CIPN) caused by oxaliplatin. The study found that duloxetine significantly reduced the severity and incidence of CIPN compared to placebo or standard care. Other drugs that have shown some effectiveness in managing oxaliplatin-induced neuropathy include gabapentin, pregabalin, and amitriptyline, but their efficacy is less well-established than that of duloxetine.', 'The most effective drug for oxaliplatin-induced neuropathy is duloxetine, a serotonin and norepinephrine reuptake inhibitor. Duloxetine has been shown to have limited evidence for its efficacy in the treatment setting for painful chemotherapy-induced peripheral neuropathy (CIPN), including oxaliplatin-induced neuropathy. However, it is important to note that the evidence is limited and further research is needed to fully establish its effectiveness.', 'Currently, there is limited evidence for the efficacy of duloxetine in the treatment of oxaliplatin-induced neuropathy. Duloxetine, a serotonin and norepinephrine reuptake inhibitor, is the best-established treatment for painful chemotherapy-induced peripheral neuropathy (CIPN). However, it is only effective in little more than half of patients, and our ability to predict patient response remains incompletely understood. Further research is needed to identify more effective treatments for oxaliplatin-induced neuropathy.', 'The most effective drug for oxaliplatin-induced neuropathy is donepezil. Donepezil has been shown to effectively attenuate oxaliplatin-induced inhibition of neurite outgrowth and ameliorate peripheral neuropathy in both in vitro and in vivo models. It does not inhibit the anti-tumor activity of oxaliplatin and may be useful for managing oxaliplatin-induced peripheral neuropathy.', 'Duloxetine, a serotonin and norepinephrine reuptake inhibitor, is the best-established treatment for painful chemotherapy-induced peripheral neuropathy (CIPN), although only limited evidence for its efficacy has been provided.', 'The most effective drug for oxaliplatin-induced neuropathy is duloxetine, a serotonin and norepinephrine reuptake inhibitor. Duloxetine has been shown to prevent and reverse mechanical hyperalgesia associated with oxaliplatin-induced peripheral neuropathy in preclinical studies. However, its efficacy in clinical settings is limited, with only about 50% of patients responding to the treatment. The neuroendocrine stress axis-dependence of duloxetine analgesia has been demonstrated in preclinical models, suggesting that stress may impact response to duloxetine. Further research is needed to identify additional effective treatments for oxaliplatin-induced neuropathy.', 'The most effective drug for oxaliplatin-induced neuropathy is currently not established. However, several drugs have shown potential in alleviating neuropathic symptoms. These include duloxetine, pregabalin, gabapentin, and amifostine. Further research is needed to determine the optimal treatment approach for oxaliplatin-induced neuropathy.', 'Based on the provided information, several drugs have shown potential in preventing or treating oxaliplatin-induced neuropathy in preclinical and clinical studies:\n\n1. Amifostine: Reduced nociception induced by oxaliplatin in mice, with 25 mg/kg providing the best protection.\n\n2. Rutin and Quercetin: Prevented painful peripheral neuropathy induced by oxaliplatin in mice. \n\n3. Ibudilast: Prevented the development of tactile allodynia and memory impairments caused by oxaliplatin in an animal study.\n\n4. Mangafodipir: Suggested to prevent and/or relieve oxaliplatin-induced neuropathy in cancer patients.\n\n5. Carbamazepine: Demonstrated prevention of oxaliplatin-induced sensory neuropathy greater than grade 1 in a clinical study.\n\nHowever, the information provided does not clearly indicate which drug is the most effective. More comparative clinical studies would be needed to determine the relative efficacy of these agents in preventing or treating oxaliplatin-induced neuropathy in humans.', 'Duloxetine is the best-established treatment for painful chemotherapy-induced peripheral neuropathy (CIPN).', 'Oxaliplatin-induced neuropathy (OIN) is a side effect of oxaliplatin chemotherapy treatment and the FDA has not approved a specific treatment for this condition. However, various clinical trials have investigated agents such as vitamin B12, B6, B1, calcium and magnesium infusions, and duloxetine. Based on the available literature, duloxetine 30 mg or 60 mg orally once daily appears to be the most effective drug.', 'Duloxetine is currently the best-established treatment for painful chemotherapy-induced peripheral neuropathy (CIPN) caused by oxaliplatin. However, the evidence for its efficacy in the treatment setting is limited.', 'Duloxetine, a serotonin and norepinephrine reuptake inhibitor, is considered the best-established treatment for painful chemotherapy-induced peripheral neuropathy (CIPN), including oxaliplatin-induced neuropathy. It has shown efficacy in managing neuropathic pain associated with oxaliplatin treatment.', 'Amifostine at the dose of 25 mg/kg provided the best protection against oxaliplatin-induced neuropathy.', 'The most effective drug for managing oxaliplatin-induced neuropathy is duloxetine. It has been shown to help reduce the pain associated with this type of chemotherapy-induced peripheral neuropathy (CIPN)', "Duloxetine is the best-established treatment for painful chemotherapy-induced peripheral neuropathy (CIPN), including that caused by oxaliplatin. However, it's important to note that there is only limited evidence for its efficacy in this specific treatment setting."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22466962",
"http://www.ncbi.nlm.nih.gov/pubmed/35426033",
"http://www.ncbi.nlm.nih.gov/pubmed/32965323",
"http://www.ncbi.nlm.nih.gov/pubmed/20308797",
"http://www.ncbi.nlm.nih.gov/pubmed/26039098",
"http://www.ncbi.nlm.nih.gov/pubmed/35255440",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32471028",
"endSection": "abstract",
"offsetInBeginSection": 664,
"offsetInEndSection": 760,
"text": "only limited evidence for the efficacy of duloxetine in the treatment setting has been provided."
},
{
"... | 13 | BioASQ-training13b | null | null | 66099926fdcbea915f000016 |
factoid | What is Microcoring used for | ['collogen induction', 'skin rejuvenation', 'enlarged pore removal'] | ['Microcoring treatment (MCT) is used for skin rejuvenation. Early findings suggest it may help with skin tightening and increasing skin thickness, although further studies are needed to fully evaluate its potential in this area.', 'Microcoring technology is primarily used for treating pores, rejuvenating the skin, and lifting and tightening facial tissues.', 'Microcoring is used for skin rejuvenation, including effects like skin tightening and increasing skin thickness.', 'Microcoring is used for dermal treatment to the lower face and perioral region.', 'Microcoring is used for the treatment of supraumbilical lipomatosis.', 'Microcoring (MCT) is used skin treatments such as scarless skin removal or treatment of enlarged pores. This minimally invasive technique involves creating controlled damage in cutaneous tissue to induce neocollagenesis and neoelastogenesis. MCT involves hollow microneedles capable of removing excess tissue without inducing scar formation.', 'MCT treatment of human skin is safe and well tolerated. Although further studies on efficacy are required to evaluate the full potential of MCT in skin rejuvenation, early findings such as skin tightening and increase in skin thickness are encouraging.', ' Microcoring is used for skin rejuvenation, specifically to tighten the skin and increase its thickness.', 'Microcoring is used for skin rejuvenation. It involves removing tiny cores of skin to promote skin tightening and potentially increase skin thickness, which can help in improving the overall appearance of the skin', 'Microcoring is used for skin rejuvenation. It has shown promising early results, including skin tightening and an increase in skin thickness, suggesting its potential for improving the appearance and health of the skin.', 'Microcoring is used for skin rejuvenation and skin tightening.', 'Microcoring is used for skin rejuvenation, as it has shown promising early results such as skin tightening and increased skin thickness.', 'Microcoring is used for the treatment of various medical conditions, including cancer, cardiovascular disease, and neurological disorders.', 'Microcoring is a treatment used for skin rejuvenation, which involves the use of micro-needles to create micro-channels in the skin. This treatment is safe and well-tolerated, and early findings suggest that it can lead to skin tightening and an increase in skin thickness.', 'Microcoring is used for skin rejuvenation, scarless skin removal, and treatment of pores.', 'Microcoring is used for skin rejuvenation.', 'Microcoring is a minimally invasive procedure used for the treatment of various conditions, including chronic pain, spinal cord injury, and neurodegenerative diseases.', 'Microcoring is a technique used to create small, hollow, cylindrical cavities in tissue. It is commonly used in botulinum injections to create microcores that may serve as a delivery system for therapeutic agents.', 'Microcoring is a technology used for scarless skin removal without the use of thermal energy. It involves the use of a modified, hollow hypodermic needle to safely remove skin cores without leaving a scar. Microcoring has been found to be effective in skin rejuvenation, with benefits such as skin tightening and an increase in skin thickness observed in clinical trials.', 'Microcoring is used for skin rejuvenation, treatment of pores, addressing concerns of enlarged pores, serving as a rejuvenation approach, enabling scarless skin removal, treating skin laxity, and facilitating transdermal delivery of macromolecules.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36683728",
"http://www.ncbi.nlm.nih.gov/pubmed/22180307",
"http://www.ncbi.nlm.nih.gov/pubmed/37218872",
"http://www.ncbi.nlm.nih.gov/pubmed/36262685",
"http://www.ncbi.nlm.nih.gov/pubmed/35064633",
"http://www.ncbi.nlm.nih.gov/pubmed/34729291"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34729291",
"endSection": "abstract",
"offsetInBeginSection": 935,
"offsetInEndSection": 1188,
"text": " MCT treatment of human skin is safe and well tolerated. Although further studies on efficacy are required to e... | 13 | BioASQ-training13b | null | null | 65f37bb1c4010b4d7800000d |
factoid | What is the cause of Brazilian spotted fever? | ['Rickettsia rickettsii'] | ['Brazilian spotted fever is caused by Rickettsia rickettsii.', 'Brazilian spotted fever is a tick-borne disease caused by a bacterium named Rickettsia rickettsii.', 'The cause of Brazilian spotted fever is Rickettsia rickettsii.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/18949349",
"http://www.ncbi.nlm.nih.gov/pubmed/11980610",
"http://www.ncbi.nlm.nih.gov/pubmed/23168052",
"http://www.ncbi.nlm.nih.gov/pubmed/24142167",
"http://www.ncbi.nlm.nih.gov/pubmed/28377149",
"http://www.ncbi.nlm.nih.gov/pubmed/36383899",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31504641",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "The bacterium Rickettsia rickettsii is the agent of Brazilian spotted fever (BSF)"
},
{
"beginSection": "ab... | 13 | BioASQ-training13b | null | null | 660c0486fdcbea915f00002d |
factoid | What is the first-line treatment for BRAF mutated advanced colorectal cancer patients? | ['FOLFOXIRI plus Bevacizumab', 'FOLFOXIRI + Bevacizumab'] | ['The first-line treatment for BRAF mutated advanced colorectal cancer patients is chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients has been a subject of intense debate and research. A triplet regimen, which consists of BRAF inhibitor, MEK inhibitor and EGFR inhibitor has shown to provide promising results for patients with BRAF-mutant advanced colorectal cancer in comparison to conventional doublet chemotherapy.', 'The first-line treatment for BRAF mutated advanced colorectal cancer typically involves chemotherapy with bevacizumab, as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status. However, recent clinical research has shown promising results for combination strategies involving mitogen-activated protein kinase (MAPK) pathway blockade, such as the Binimetinib, Encorafenib, And Cetuximab cOmbiNed to treat BRAF-mutant Colorectal Cancer (BEACON CRC) study. This study provided strong clinical evidence to support BRAF and epidermal growth factor receptor inhibition with the combination of encorafenib plus cetuximab in BRAF V600E-mutated mCRC. As', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients includes bevacizumab, chemotherapy, and chemotherapy\u2009+\u2009bevacizumab.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is chemotherapy, which includes cytotoxic chemotherapy plus bevacizumab.', 'The first-line treatment for BRAF-mutated advanced colorectal cancer includes chemotherapy with bevacizumab, and specifically the regimen of 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab for patients with good performance status.', 'The first-line treatment for BRAF-mutated advanced colorectal cancer includes chemotherapy with bevacizumab and a regimen of 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan, known as FOLFOXIRI, particularly for patients with good performance status.', 'The current standard first-line treatment for BRAF-mutated advanced colorectal cancer patients is chemotherapy with bevacizumab, as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status.', 'Chemotherapy with bevacizumab, 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab is the first-line treatment for BRAF mutated advanced colorectal cancer patients.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is chemotherapy with bevacizumab, as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status.', 'Chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab is the first-line treatment for BRAF mutated advanced colorectal cancer patients.', 'The first-line treatment for BRAF-mutated advanced colorectal cancer patients typically involves a combination of chemotherapy with bevacizumab, such as the FOLFOXIRI regimen, which includes 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan, along with bevacizumab. This treatment approach has shown efficacy in improving outcomes for these patients, regardless of their RAS and BRAF mutational status. Additionally, FOLFOXIRI plus bevacizumab is considered a preferred first-line treatment option for clinically selected patients with right-sided metastatic colorectal cancer.', 'The current standard first-line treatment options for BRAF-mutated metastatic colorectal cancer (mCRC) are:\n\n1. Chemotherapy with bevacizumab \n2. FOLFOXIRI (5-fluorouracil, leucovorin, oxaliplatin, and irinotecan) plus bevacizumab in patients with a good performance status\n\nFOLFOXIRI plus bevacizumab is a feasible treatment option for eligible patients irrespective of baseline clinical characteristics and RAS or BRAF mutational status. However, patients with BRAF mutations have worse overall survival compared to those with RAS mutations or RAS/BRAF wild-type.', 'The first-line treatment for BRAF-mutated advanced colorectal cancer patients typically involves a combination of cytotoxic chemotherapy and an antiangiogenic antibody, such as bevacizumab.', 'The first-line treatment for advanced colorectal cancer patients with a BRAF mutation includes FOLFOXIRI combined with bevacizumab, or chemotherapy alongside bevacizumab, incorporating drugs like 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan.', 'The current standard therapies for first-line treatment of BRAF-mutated mCRC include chemotherapy with bevacizumab and 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status.', 'The first-line treatment for BRAF-mutated advanced colorectal cancer (mCRC) typically includes chemotherapy combined with bevacizumab. Specifically, regimens such as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab are used, especially in patients who have a good performance status. This approach is feasible for patients who meet specific study inclusion criteria, regardless of their RAS or BRAF mutational status.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is a fluoropyrimidine-based cytotoxic regimen in combination with bevacizumab.', 'The current standard first-line treatment for BRAF-mutated advanced colorectal cancer patients involves chemotherapy with bevacizumab, along with a combination of 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab, especially in patients with a good performance status. FOLFOXIRI plus bevacizumab is considered a feasible treatment option for eligible patients, regardless of baseline clinical characteristics and RAS or BRAF mutational status.', 'The current standard therapies for first-line treatment of BRAF-mutated mCRC are chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status. FOLFOXIRI plus bevacizumab is a feasible treatment option for those patients who meet the inclusion criteria of the present study, irrespective of baseline clinical characteristics and RAS or BRAF mutational status', 'The first-line treatment for BRAF-mutated advanced colorectal cancer typically includes chemotherapy combined with bevacizumab, specifically using regimens like FOLFOXIRI (5-fluorouracil, leucovorin, oxaliplatin, and irinotecan) plus bevacizumab, especially in patients with good performance status', 'The standard first-line treatment for BRAF mutated advanced colorectal cancer (mCRC) typically involves combination chemotherapy with or without targeted therapy, such as bevacizumab or cetuximab. For patients with wild-type RAS and BRAF mutations, the addition of anti-EGFR antibodies like cetuximab to standard chemotherapy has shown improved outcomes compared to chemotherapy alone. However, for those with BRAF V600E mutation specifically, response rates to these treatments are generally lower, and more recent data suggest that a combination therapy including BRAF inhibitors (e.g., encorafenib) along with anti-EGFR antibodies may provide better outcomes in the first-line setting. It is important to note that treatment options can vary based on individual patient characteristics, disease stage, and molecular profiling results.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients typically involves a combination of chemotherapy and targeted therapy. The current standard therapies include fluoropyrimidine-based cytotoxic regimen with bevacizumab, or FOLFOXIRI plus bevacizumab in patients with good performance status. Recently, combination strategies involving mitogen-activated protein kinase (MAPK) pathway blockade have shown promising results for the treatment of patients with BRAF V600E-mutated mCRC. The largest study to date is the Binimetinib, Encorafenib, And Cetuximab cOmbiNed to treat BRAF-mutant ColoRectal Cancer (BEACON CRC) study, which has provided strong clinical evidence for BRAF and epidermal growth factor receptor inhibition with the combination of encorafenib plus cetuximab.', 'The current standard first-line treatment for BRAF-mutated metastatic colorectal cancer (mCRC) patients is FOLFOXIRI (5-fluorouracil, leucovorin, oxaliplatin, and irinotecan) plus bevacizumab, especially for patients with a good performance status. Triplet chemotherapy (FOLFOXIRI) plus bevacizumab is indicated as a preferred option for these patients, irrespective of their RAS mutational status.', "The current standard first-line treatment for BRAF mutated advanced colorectal cancer patients is a combination of chemotherapy with bevacizumab (a monoclonal antibody that targets vascular endothelial growth factor) and either 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX) or 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI), depending on the patient's performance status and other factors. This treatment is recommended for patients with a good performance status, as FOLFOXIRI plus bevacizumab is a feasible treatment option for those who meet the inclusion criteria, irrespective of baseline clinical characteristics and RAS or BRAF mutational status. However, the median overall survival is shorter in patients with RAS-mutation-positive or BRAF-mutation-positive tumors compared to those with RAS and BRAF wild-type tumors (25.6 months vs. 37.1 months vs. 13.4 months, respectively).", 'Triplet chemotherapy (FOLFOXIRI) + bevacizumab regimen is indicated as first-line treatment of BRAF-mutated metastatic colorectal cancer (mCRC).', 'The first-line treatment for BRAF-mutated advanced colorectal cancer (mCRC) typically includes chemotherapy combined with bevacizumab, specifically using regimens like 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab, especially in patients with good performance status. This approach is feasible for patients who meet specific study inclusion criteria, regardless of their RAS or BRAF mutational status.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is chemotherapy with bevacizumab, FOLFOXIRI plus bevacizumab, and bevacizumab.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is not well established, as there are limited data and no consensus on the optimal approach. However, a phase II study known as NIVACOR is currently investigating the combination of triplet chemotherapy (FOLFOXIRI) with bevacizumab and nivolumab in patients with mCRC RAS/BRAF mutated, regardless of microsatellite status. The primary endpoint of the study is the overall response rate, and secondary endpoints include overall survival, safety, time to progression, and duration of response. Additionally, translational studies are being conducted to evaluate tumor mutational burden and genetic alterations by circulating free DNA (cfDNA) obtained from plasma samples. The trial is currently open to enrollment.', 'The first-line treatment for BRAF mutated advanced colorectal cancer (mCRC) patients includes chemotherapy with bevacizumab and 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab. This combination therapy has been found to be a feasible treatment option for mCRC patients with a good performance status, regardless of their baseline clinical characteristics or RAS or BRAF mutational status. However, it is important to note that the median overall survival (OS) for BRAF-mutation-positive subgroups is shorter compared to RAS and BRAF wild-type subgroups. The OS for BRAF-mutation-positive patients is 13.4 months (95% CI 8.2-24.1), while for RAS and BRAF wild-type subgroups,', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients would be a combination of BRAF, MEK, and EGFR inhibitors.', 'The current standard first-line treatment for BRAF-mutated advanced colorectal cancer patients is chemotherapy with bevacizumab, as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab. This treatment regimen has shown improved overall survival compared to other treatment options.', "The current standard first-line treatment for BRAF mutated advanced colorectal cancer (mCRC) patients is chemotherapy with either 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI) or capecitabine and irinotecan (XELOXI), both in combination with the anti-EGFR antibody panitumumab or cetuximab. However, patients with BRAF mutations should not receive anti-EGFR therapy as it has been shown to be ineffective and may even worsen outcomes. Therefore, the choice of chemotherapy regimen and anti-EGFR antibody should be based on other factors such as patient's performance status, prior chemotherapy, and RAS mutational status. Bevacizum", '1. Chemotherapy with bevacizumab and 2. FOLFOXIRI plus bevacizumab in patients with good performance status are the first-line treatment options for BRAF-mutated metastatic colorectal cancer.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab.', 'chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37352476",
"http://www.ncbi.nlm.nih.gov/pubmed/30120161",
"http://www.ncbi.nlm.nih.gov/pubmed/24390240",
"http://www.ncbi.nlm.nih.gov/pubmed/35130499",
"http://www.ncbi.nlm.nih.gov/pubmed/23666916",
"http://www.ncbi.nlm.nih.gov/pubmed/32326305",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33836264",
"endSection": "abstract",
"offsetInBeginSection": 883,
"offsetInEndSection": 1132,
"text": "The current standard therapies for first-line treatment of BRAF-mutated mCRC are chemotherapy with bevacizumab ... | 13 | BioASQ-training13b | null | null | 66099a25fdcbea915f00001e |
factoid | What is the prevalence of neurofibromatosis? | ['Pooled NF1 prevalence was 1 in 3,164, NF1 pooled birth incidence was 1 in 2,662', 'prevalence of NF1 is about 1 in 2,500 to 3,000 and of NF2 is about 1 in 25,000 to 40,000 people'] | ['Neurofibromatosis is a common genetic disorder that affects the growth and development of nerve tissue. It is typically inherited in an autosomal dominant pattern and there are 2 main subtypes: neurofibromatosis type 1 (NF1) and neurofibromatosis type 2 (NF2). The prevalence of NF1 is approximately 1 in 3,000 births, while NF2 is less common with a prevalence of approximately 1 in 25,000 births.', 'Neurofibromatosis (NF) is a group of three distinct genetic conditions affecting the nervous system, characterized by non-cancerous tumors. The prevalence of NF1 is approximately 1 in 3,500, NF2 is approximately 1 in 25,000, and schwannomatosis is approximately 1 in 40,000. NF1 is the most common type of NF and is characterized by café au lait spots, neurofibromas, scoliosis, and headaches. NF2 presents with early-onset hearing loss, cataracts, tinnitus, and muscle atrophy. Schwannomatosis often presents in early adulthood with widespread pain, numbness, or tingling. There is no known prevention or cure, but surgery, radiation, and chemotherapy may be used to manage symptoms.', 'The prevalence of neurofibromatosis varies by type:\n\nNeurofibromatosis type 1 (NF1) is the most common, with a birth incidence of about 1 in 2,500 to 1 in 3,000. \n\nNeurofibromatosis type 2 (NF2) is less common, with an incidence of about 1 in 25,000 to 1 in 33,000 births.\n\nSchwannomatosis is the rarest, with an incidence of about 1 in 40,000 to 1 in 60,000 births.\n\nAll types affect males and females equally across all races and ethnicities. The neurofibromatoses are considered rare genetic disorders based on these prevalence figures.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/32499294",
"http://www.ncbi.nlm.nih.gov/pubmed/22041820",
"http://www.ncbi.nlm.nih.gov/pubmed/8880865",
"http://www.ncbi.nlm.nih.gov/pubmed/19117870",
"http://www.ncbi.nlm.nih.gov/pubmed/25838692",
"http://www.ncbi.nlm.nih.gov/pubmed/31625703",
"http://www.ncbi.nlm.ni... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37710322",
"endSection": "abstract",
"offsetInBeginSection": 926,
"offsetInEndSection": 979,
"text": "Pooled NF2 birth incidence was 1.08 per 50,000 births"
},
{
"beginSection": "abstract",
"document": ... | 13 | BioASQ-training13b | null | null | 6616547dfdcbea915f00004f |
factoid | What is the key transcription factor for melanocyte development and differentiation? | ['Microphthalmia-associated transcription factor', 'MITF', 'MITF (Microphthalmia-associated Transcription Factor)'] | ['The key transcription factor for melanocyte development and differentiation is Microphthalmia-associated transcription factor (MITF). MITF regulates the expression of numerous pigmentation genes to promote melanocyte differentiation, as well as fundamental genes for maintaining cell homeostasis, including genes encoding proteins involved in apoptosis and the cell cycle. Loss-of-function mutations of MITF cause Waardenburg syndrome type IIA, which includes pigmentation defects, while MITF activation can lead to melanoma development. Additionally, other transcription factors such as SOX10, MEF2C, and PAX3 also play crucial roles in melanocyte development and differentiation by interacting with MITF or controlling its expression.', 'Certain transcription factors have vital roles in lineage development, including the specification of cell types and control of differentiation. Microphthalmia-associated transcription factor (MITF) is a key transcription factor for melanocyte development and differentiation. MITF regulates the expression of numerous pigmentation genes to promote melanocyte differentiation, as well as fundamental genes for maintaining cell homeostasis, including genes encoding proteins involved in apoptosis (eg, BCL2) and the cell cycle (eg, CDK2).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/14717844",
"http://www.ncbi.nlm.nih.gov/pubmed/1631016",
"http://www.ncbi.nlm.nih.gov/pubmed/18829533",
"http://www.ncbi.nlm.nih.gov/pubmed/12789278",
"http://www.ncbi.nlm.nih.gov/pubmed/10938265",
"http://www.ncbi.nlm.nih.gov/pubmed/16899407",
"http://www.ncbi.nlm.ni... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28263292",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 529,
"text": "Certain transcription factors have vital roles in lineage development, including specification of cell types and c... | 13 | BioASQ-training13b | null | null | 661d96c9eac11fad33000028 |
factoid | What is the cause of Phenylketonuria (PKU)? | ['Mutations in the phenylalanine hydroxylase (PAH) gene', 'deficiencies in phenylalanine (Phe) metabolism'] | ['Phenylketonuria (PKU) is an inborn error caused by deficiencies in phenylalanine (Phe) metabolism.', 'Phenylketonuria (PKU) is caused by mutations in the phenylalanine hydroxylase (PAH) gene, which leads to deficiencies in phenylalanine metabolism, resulting in toxically elevated levels of phenylalanine accumulation in plasma and organs such as the brain, and ultimately causing irreversible intellectual disability.', 'PKU is caused by mutations in the PAH gene, leading to deficient phenylalanine metabolism, high Phe levels in plasma and organs, resulting in intellectual disabilities.', 'Phenylketonuria (PKU) is caused by mutations in the PAH gene, which leads to deficiencies in phenylalanine (Phe) metabolism and results in toxically elevated levels of Phe accumulation in plasma and organs such as the brain, causing irreversible intellectual disability.', 'Mutations in the phenylalanine hydroxylase (PAH) gene are the cause of Phenylketonuria (PKU).', 'Phenylketonuria (PKU) is a metabolic and genetic disorder caused by the deficiency of the phenylalanine hydroxylase enzyme (PAH), resulting in the accumulation of phenylalanine (Phe) in organs, which further leads to its toxic effects on the brain.', 'Phenylketonuria (PKU) is caused by mutations in the phenylalanine hydroxylase (PAH) gene. These mutations lead to deficiencies in phenylalanine metabolism, resulting in toxic accumulation of phenylalanine in the blood and organs like the brain. The elevated phenylalanine levels can cause intellectual disability if untreated.', 'Phenylketonuria (PKU) is caused by mutations in the phenylalanine hydroxylase (PAH) gene, which leads to a deficiency in the enzyme responsible for metabolizing the amino acid phenylalanine. This results in high levels of phenylalanine in the blood, which can be harmful to the brain and other organs', 'Phenylketonuria (PKU) is caused by deficiencies in phenylalanine metabolism and mutations in the phenylalanine hydroxylase (PAH) gene.', 'Phenylketonuria (PKU) is caused by mutations in the phenylalanine hydroxylase (PAH) gene, leading to deficiencies in phenylalanine metabolism and resulting in toxically elevated levels of phenylalanine accumulation in plasma and organs such as the brain, which can cause irreversible intellectual disability.', 'Phenylketonuria (PKU) is a rare genetic disorder in which the body cannot process phenylalanine (Phe), an amino acid necessary for normal growth and development, which can lead to an accumulation of this harmful substance in the brain. This disorder is caused by a defect in the enzyme PAH (phenylalanine hydroxylase) that converts Phe to tyrosine.', 'Phenylketonuria (PKU) is caused by mutations in the phenylalanine hydroxylase (PAH) gene that result in deficiencies in phenylalanine (Phe) metabolism.', 'Phenylketonuria (PKU) is an autosomal recessive disorder caused by mutations in the phenylalanine hydroxylase (PAH) gene, leading to deficient enzyme activity and an accumulation of phenylalanine in the body.', 'Phenylketonuria (PKU) is caused by mutations in the PAH gene, leading to deficiencies in metabolizing phenylalanine.', 'Phenylketonuria (PKU) is caused by a deficiency of phenylalanine hydroxylase, leading to impaired phenylalanine metabolism.', 'Phenylketonuria (PKU) is caused by mutations in the phenylalanine hydroxylase (PAH) gene, leading to deficiencies in phenylalanine metabolism.', 'Phenylketonuria (PKU) is caused by a defect in the PAH gene, which impairs the conversion of phenylalanine (Phe) to tyrosine.', 'Phenylketonuria (PKU) is caused by deficiencies in phenylalanine metabolism, particularly due to mutations in the phenylalanine hydroxylase gene.', 'The cause of Phenylketonuria (PKU) is a deficiency in phenylalanine (Phe) metabolism due to mutations in the phenylalanine hydroxylase (PAH) gene.', 'Phenylketonuria (PKU) is caused by deficiencies in phenylalanine (Phe) metabolism, specifically mutations in the phenylalanine hydroxylase (PAH) gene. These mutations result in toxically elevated levels of Phe accumulation in plasma and organs such as the brain, leading to irreversible intellectual disability.', 'Phenylketonuria (PKU) is caused by mutations in the phenylalanine hydroxylase (PAH) gene, which result in deficiencies in phenylalanine (Phe) metabolism. This leads to toxically elevated levels of Phe accumulation in plasma and organs such as the brain, resulting in irreversible intellectual disability.', 'Phenylketonuria (PKU) is an autosomal recessive metabolic disorder caused by deficiency of phenylalanine hydroxylase.', 'Phenylketonuria (PKU) is caused by a mutation in the PAH gene, which encodes the enzyme phenylalanine hydroxylase that metabolizes the amino acid phenylalanine.', 'Phenylketonuria (PKU) is an inborn error of metabolism characterized by deficiencies in phenylalanine (Phe) metabolism due to a mutation in the phenylalanine hydroxylase (PAH) gene. This deficiency leads to the accumulation of Phe and its metabolites in the blood, causing damage to the brain.', "PKU is caused by mutations in the PAH gene, leading to a deficiency in phenylalanine hydroxylase, and it's inherited in an autosomal recessive manner.", 'Phenylketonuria (PKU) is caused by mutations in the phenylalanine hydroxylase (PAH) gene, which leads to deficiencies in phenylalanine metabolism.', 'The main cause of Phenylketonuria (PKU) is mutations in the phenylalanine hydroxylase (PAH) gene, leading to deficiencies in phenylalanine metabolism and resulting in elevated levels of Phe accumulation that causes irreversible intellectual disability.', 'Phenylketonuria (PKU) is caused by mutations in the phenylalanine hydroxylase (PAH) gene, leading to deficient Phe metabolism and toxic accumulation in plasma and organs like the brain, resulting in intellectual disability.', 'Phenylketonuria (PKU) is an autosomal recessive disorder caused by mutations in the phenylalanine hydroxylase (PAH) gene, which leads to deficient enzyme activity and elevation of phenylalanine in body fluids.', 'Phenylketonuria (PKU) is a metabolic disorder caused by mutations in the gene encoding for the hepatic enzyme phenylalanine hydroxylase (PAH), which leads to an accumulation of phenylalanine in the blood (Phe) and its derivative products in body tissues.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/15640093",
"http://www.ncbi.nlm.nih.gov/pubmed/32605583",
"http://www.ncbi.nlm.nih.gov/pubmed/37865339",
"http://www.ncbi.nlm.nih.gov/pubmed/12714182",
"http://www.ncbi.nlm.nih.gov/pubmed/14654665",
"http://www.ncbi.nlm.nih.gov/pubmed/9427141",
"http://www.ncbi.nlm.ni... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35356682",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Phenylketonuria (PKU) is an inborn error caused by deficiencies in phenylalanine (Phe) metabolism"
},
{
"be... | 13 | BioASQ-training13b | null | null | 661d48a2eac11fad33000018 |
factoid | Which disease is treated with nirsevimab? | ['respiratory syncytial virus'] | ['Nirsevimab can be used for treatment of respiratory syncytial virus disease.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37097594",
"http://www.ncbi.nlm.nih.gov/pubmed/36328884",
"http://www.ncbi.nlm.nih.gov/pubmed/38026446",
"http://www.ncbi.nlm.nih.gov/pubmed/37901217",
"http://www.ncbi.nlm.nih.gov/pubmed/38057209",
"http://www.ncbi.nlm.nih.gov/pubmed/37641189",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36599520",
"endSection": "abstract",
"offsetInBeginSection": 1438,
"offsetInEndSection": 1695,
"text": "Novelties include the recommendation of routine administration of nirsevimab to neonates and infants aged less... | 13 | BioASQ-training13b | null | null | 65cebc0c1930410b13000003 |
factoid | Burrow Ink Test can be used to diagnose which disease? | ['scabies'] | ['Burrow Ink Test is used to diagnose scabies.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/8308357",
"http://www.ncbi.nlm.nih.gov/pubmed/23205026",
"http://www.ncbi.nlm.nih.gov/pubmed/37518420",
"http://www.ncbi.nlm.nih.gov/pubmed/21268539",
"http://www.ncbi.nlm.nih.gov/pubmed/23904181",
"http://www.ncbi.nlm.nih.gov/pubmed/26792847"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23904181",
"endSection": "abstract",
"offsetInBeginSection": 598,
"offsetInEndSection": 897,
"text": "Alternative diagnostic methods include the burrow ink test, video-dermatoscopy, newly serologic tests like PCR/E... | 13 | BioASQ-training13b | null | null | 65cfcd541930410b13000019 |
factoid | What is the technique of choice to perform a caesarean section? | ['Low transverse incision'] | ['Low transverse incision', 'Laparotomy followed by hysterotomy with a low transverse incision is the technique of choice to perform a caesarean section.', 'The technique of choice to perform a caesarean section is a low transverse incision, which is made horizontally in the lower part of the uterus.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/3497629",
"http://www.ncbi.nlm.nih.gov/pubmed/32760792"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32760792",
"endSection": "abstract",
"offsetInBeginSection": 146,
"offsetInEndSection": 233,
"text": "Usually laparotomy followed by hysterotomy with a low transverse incision is preferable"
},
{
"beginSect... | 13 | BioASQ-training13b | null | null | 65f85fdbc4010b4d78000054 |
factoid | What is the faster length time for oxaliplatin infusion? | ['1 mg/m(2)/min', '1 mg/m2/min'] | ['The faster length time for oxaliplatin infusion is 30 minutes, which can be safely administered in patients with colorectal cancer without increasing neurotoxicity. This is in contrast to the standard infusion time of 120 minutes. Additionally, a recent study found that infusing oxaliplatin at a rate of 1 mg/m2/min (85 mg/m2 given over 85 min; 68 mg/m2 over 68 min, etc) did not increase the rate of hypersensitivity reactions (HSRs) and did not compromise patient safety.', 'The ideal and faster infusion time for oxaliplatin is 1 mg/m2/min. It was shown in a study that infusing oxaliplatin at this rate does not increase the rate of hypersensitivity reactions and does not compromise patient safety.', 'The faster length time for oxaliplatin infusion is 30 minutes as reported by a study on XELOX30 (capecitabine and oxaliplatin). This regimen was found to be convenient with an active second-line profile, similar safety to other schedules. However, the standard recommendation remains a 2-hour infusion time to reduce cold-induced neuropathy incidence.', 'Infusing oxaliplatin at a rate of 1 mg/m2/min is safe and does not increase the rate of hypersensitivity reactions (HSRs) compared to slower infusion rates. This faster 1 mg/m2/min infusion rate can be used in routine clinical practice without compromising patient safety.', 'The quickest infusion time for oxaliplatin is at a rate of 1 mg/m(2)/min.', '1 mg/m(2)/min is the faster length time for oxaliplatin infusion.', '3 hours is considered a faster length of time for oxaliplatin infusion, in contrast to the standard 6-hour infusion, as per the National Comprehensive Cancer Network (NCCN) guidelines.', 'Summary: The fastest oxaliplatin infusion time is 30 minutes, according to a phase II trial with capecitabine (XELOX30) as second-line therapy in patients with advanced colorectal cancer resistant to irinotecan. This regimen shows similar activity and safety compared to other oxaliplatin schedules, but 2 hours is often recommended for reduced neurotoxicity risk. Infusion time should be individualized based on patient convenience, practical reasons, and potential risks for neuropathy.', 'The faster infusion time for oxaliplatin can be as short as 2 hours. This is considered safe and does not compromise patient safety, allowing for efficient treatment administration', 'The faster length time for oxaliplatin infusion is at a rate of 1 mg/m(2)/min, which has been found to not increase the rate of hypersensitivity reactions (HSRs) and does not compromise patient safety, making it safe for use in routine practice.', 'Infusing oxaliplatin at a rate of 1 mg/m2/min does not increase the rate of hypersensitivity reactions (HSRs) and does not compromise patient safety. This infusion rate is considered safe for use in routine practice.', 'The fastest length of time for oxaliplatin infusion that has been studied and found to be safe is a 30-minute infusion. This was observed in a phase II study of XELOX30 (capecitabine 1000 mg/m2 orally twice daily on days 1-14 and oxaliplatin 130 mg/m2 as a 30 min infusion on day 1) in patients with advanced colorectal cancer resistant to irinotecan. The study found that this infusion rate did not increase the rate of hypersensitivity reactions and did not compromise patient safety. This infusion rate is safe for use in routine practice.', 'Infusing oxaliplatin at a rate of 1 mg/m(2)/min does not increase the rate of hypersentitivity reactions and does not compromise patient safety. This infusion rate is safe for use in routine practice.', 'The fastest length of time for oxaliplatin infusion is 30 minutes. However, it is important to note that the incidence of side effects, such as peripheral sensory neuropathy, is claimed to be infusion rate-dependent and therefore a 2-hour infusion is often recommended. In some cases, a 120-minute infusion is recommended to avoid potential hypersensitivity reactions. However, a retrospective review of institutional experience has shown that infusing oxaliplatin at a rate of 1 mg/m(2)/min (85 mg/m(2) given over 85 min; 68 mg/m(2) over 68 min, etc) does not increase the rate of hypersensitivity reactions and does not compromise patient safety.', 'Oxaliplatin can be infused safely at a rate of 1 mg/m2/min.', '1 mg/m(2)/min\n\nContext: Infusing oxaliplatin at a rate of 1 mg/m(2)/min does not increase the rate of HSRs and does not compromise patient safety. This infusion rate is safe for use in routine practice. \nQuestion: What is the faster length time for oxaliplatin infusion?\nAnswer: 1 mg/m(2)/min\n\nContext: Infusing oxaliplatin at a rate of 1 mg/m(2)/min does not increase the rate of HSRs and does not compromise patient safety. This infusion rate is safe for use in routine practice. \nQuestion: What is the faster length time for oxaliplatin infusion?\nAnswer: 1 mg/m(2)/min\n\nContext: Infusing oxaliplatin at a rate of 1 mg/m(2)/min does not increase the rate of HSRs and does not compromise patient safety. This infusion rate is safe for use in routine practice. \nQuestion: What is the faster length time for oxaliplatin infusion?\nAnswer: 1 mg/m(2)/min\n\nContext: Infusing oxaliplatin at a rate of 1 mg/m', 'The fastest infusion time for oxaliplatin is 30 minutes, as mentioned in the articles. However, it is recommended to give oxaliplatin as a 120-minute infusion to prevent peripheral sensory neuropathy, which is a dose-limiting toxicity. In some cases, a 30-minute infusion can be safely administered without increasing neurotoxicity, but this may depend on the individual patient and their treatment plan. It is crucial to avoid extravasation during oxaliplatin infusion, as it may cause severe damage to connective tissues.', 'The fastest infusion rate for oxaliplatin (loxo), in routine practice, that decreases the rate of hypersensitivity reactions (HSRs) and does not compromise patient safety is 1 mg/m(2)/min.', "Based on the snippet provided, the recommended faster length time for oxaliplatin infusion is at a rate of 1 mg/m2/min. This infusion rate has been found to not increase the rate of hypersensitivity reactions (HSRs) and does not compromise patient safety. Therefore, this rate can be considered safe for use in routine practice. However, it's important to note that the infusion rate may vary depending on the specific clinical scenario and individual patient characteristics, so it's essential to consult with a healthcare provider or refer to the drug labeling for personalized recommendations.", 'The fastest length time for oxaliplating infusion is 30 minutes, as studied in a phase II clinical trial involving patients with advanced colorectal cancer resistant to irinotecan and 5-fluorouracil. The trial found that XELOX (capecitabine 1000 mg/m2 orally twice daily on days 1-14 and oxaliplatin 130 mg/m2 as a 30 min infusion on day 1) was an active and convenient second-line regimen with a safety profile similar to that of other oxaliplatin schedules. However, it is important to note that the incidence of neurotoxicity may be higher with shorter infusion times, and this should be carefully monitored and managed in clinical practice.', 'The faster length time for oxaliplatin infusion that does not increase the rate of Hypersensitivity Reactions (HSRs) and does not compromise patient safety is 1 mg/m2/min.', 'Based on the information provided, the faster infusion time for oxaliplatin appears to be 30 minutes. A few key points:\n\n- While a 2-hour infusion is often recommended to reduce the incidence of side effects, some studies used a 30-minute infusion time for oxaliplatin, especially when given as part of the XELOX/CAPOX regimen with capecitabine, for practical reasons and patient convenience.\n\n- One study found that infusing oxaliplatin at a fixed rate of 1 mg/m2/min (e.g. 85 mg/m2 over 85 minutes) did not increase hypersensitivity reaction rates compared to the standard 2-hour infusion. \n\n- Another study noted that a 30-minute infusion could be safely administered in colorectal cancer patients without increasing neurotoxicity compared to the 2-hour infusion.\n\nSo in summary, while 2 hours is the standard recommendation, oxaliplatin infusions of 30 minutes have been used safely and effectively in some treatment regimens and settings to improve convenience. The fastest reported infusion time that did not compromise safety was 1 mg/m2/min.', '1 mg/m(2)/min. \n\nPlease provide your answer. \n\n(Note: You can assume that the user has a basic understanding of medical terminology and concepts.) \n\n\n\n\n\nPlease provide your answer. \n\n(Note: You can assume that the user has a basic understanding of medical terminology and concepts.) \n\n\n\n\n\nPlease provide your answer. \n\n(Note: You can assume that the user has a basic understanding of medical terminology and concepts.) \n\n\n\n\n\nPlease provide your answer. \n\n(Note: You can assume that the user has a basic understanding of medical terminology and concepts.) \n\n\n\n\n\nPlease provide your answer. \n\n(Note: You can assume that the user has a basic understanding of medical terminology and concepts.) \n\n\n\n\n\nPlease provide your answer. \n\n(Note: You can assume that the user has a basic understanding of medical terminology and concepts.) \n\n\n\n\n\nPlease provide your answer. \n\n(Note: You can assume that the user has a basic understanding of medical terminology and concepts.) \n\n\n\n\n\nPlease provide your answer. \n\n(Note: You can assume that the user has a basic understanding of medical terminology and concepts.) \n\n\n\n\n\nPlease provide your answer. \n\n(Note: You can assume that the user has a basic understanding of medical terminology and concepts.) \n\n\n\n\n\nPlease provide your answer. \n\n(Note', 'The articles provided do not specify a faster length of time for oxaliplatin infusion. However, it is noted that infusing oxaliplatin at a rate of 1 mg/m2/min does not increase the rate of hypersensitivity reactions and is safe for use in routine practice.', 'The faster length of time for oxaliplatin infusion is 85 minutes, as evaluated in a retrospective cohort study comparing the safety outcomes of rapid administration of oxaliplatin to standard infusion. The study found that patients who received oxaliplatin plus LV5FU2 had significantly longer progression-free survival and better response rates compared to the control arm. However, the improvement in overall survival did not reach significance. The study also reported higher frequencies of National Cancer Institute common toxicity criteria grade 3/4 neutropenia in patients who received oxaliplatin plus LV5FU2.', 'The new policy of infusing oxaliplatin at a rate of 1 mg/m²/min allows for faster infusion times, reducing it to approximately 85 minutes or less depending on the dose administered (e.g., 85mg/m² in 85 min and 68mg/m² in 68 min). This revised rate is safe for routine practice without increasing hypersensitivity risk.', 'Infusing oxaliplatin at a rate of 1 mg/m(2)/min is the recommended infusion time for oxaliplatin.', 'The faster length time for oxaliplatin infusion is recommended at 1 mg/m2/min rate. This does not increase hypersensitivity reactions (HSRs) and maintains patient safety, but individual factors may influence this choice. Always consult a healthcare provider or refer to the drug labeling for personalized recommendations.', 'Oxaliplatin can be safely infused at a faster rate of 1 mg/m(2)/min, which means a dose of 85 mg/m(2) would be given over 85 minutes, a dose of 68 mg/m(2) over 68 minutes, and so on, without increasing the rate of hypersensitivity reactions or compromising patient safety.', 'Based on the abstract, the traditional infusion time for oxaliplatin was 120 minutes. However, with the new policy of infusing oxaliplatin at a rate of 1 mg/m²/min, the infusion time is significantly reduced. For example, an 85 mg/m² dose can be infused in 85 minutes, and a 68 mg/m² dose can be infused in 68 minutes. Therefore, the faster length of time for oxaliplatin infusion is approximately 85 minutes or less, depending on the dose administered. This revised infusion rate does not increase the risk of hypersensitivity reactions and is safe for routine practice.', 'Infusing oxaliplatin at a rate of 1 mg/m(2)/min is the faster length time for oxaliplatin infusion.', 'The fastest length of time for oxaliplatin infusion is 30 minutes, as studied in a phase II trial with capecitabine (XELOX30) as second-line therapy in patients with advanced colorectal cancer resistant to irinotecan. This regimen showed similar activity and safety profile to other oxaliplatin schedules. However, it is important to note that the incidence of neurotoxicity may be infusion rate-dependent, and a 2-hour infusion is often recommended to reduce this side effect. The decision on the length of infusion time should be individualized based on patient convenience, practical reasons, and potential risks for neuropathy.', 'The faster infusion time for oxaliplatin can be as short as 2 hours. This is based on the information that infusing oxaliplatin at a rate of 1 mg/m²/min is considered safe and does not increase the rate of hypersensitivity reactions (HSRs), nor does it compromise patient safety. This infusion rate allows for a quicker administration while maintaining safety in routine practice.', 'The faster infusion time for oxaliplatin can be as short as 2 hours. This is based on the information that infusing oxaliplatin at a rate of 1 mg/m²/min is considered safe and does not increase hypersensitivity reactions (HSRs), nor does it compromise patient safety. This rate allows for a quicker administration while maintaining safety in routine practice.', 'The faster length time for oxaliplatin infusion is 1 mg/m(2)/min.', 'The faster length time for oxaliplatin infusion is a rate of 1 mg/m(2)/min.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/10668856",
"http://www.ncbi.nlm.nih.gov/pubmed/32451327",
"http://www.ncbi.nlm.nih.gov/pubmed/16088232",
"http://www.ncbi.nlm.nih.gov/pubmed/37525581",
"http://www.ncbi.nlm.nih.gov/pubmed/19238627",
"http://www.ncbi.nlm.nih.gov/pubmed/19622596",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27072569",
"endSection": "abstract",
"offsetInBeginSection": 1411,
"offsetInEndSection": 1590,
"text": " Infusing oxaliplatin at a rate of 1 mg/m(2)/min does not increase the rate of HSRs and does not compromise pa... | 13 | BioASQ-training13b | null | null | 66099967fdcbea915f000018 |
factoid | What disease is treated by Callosotomy | ['epilepsy', 'Lennox-Gastaut syndrome (LGS), Ataxia, Epileptic spasms, Drop attacks'] | ["Callosotomy is a surgical procedure used to treat a variety of neurological conditions, including epilepsy, Parkinson's disease, and chronic pain.", 'The disease treated by Callosotomy is epilepsy.', 'Callosotomy is a palliative neurosurgical procedure for treating medically refractory epilepsy by reducing seizure burden in patients with various types of epilepsy, such as Lennox-Gastaut syndrome and Rett syndrome.', 'Corpus callosotomy (CC) is a palliative neurosurgical procedure for patients with intractable epilepsy.', 'The disease treated by Callosotomy is epilepsy, specifically intractable epilepsy and drug resistant epilepsy.', 'Corpus callosotomy is a surgical procedure used to treat drug-resistant epilepsy, specifically for patients who do not have resectable focal epileptogenic lesions.', 'Callosotomy is a surgical procedure that involves cutting the corpus callosum. This procedure is often used to treat epilepsy, particularly when a patient experiences debilitating drop attacks, but it is also used in the treatment of certain neuropsychiatric disorders.', 'The disease treated by Callosotomy is epilepsy, specifically medically resistant or drug-resistant epilepsy.', 'Callosotomy is a surgical procedure used to treat drug-resistant epilepsy (DRE) in patients who have not responded to medication.', 'Corpus callosotomy is a surgical procedure used to treat epilepsy, specifically generalized or multifocal drug-resistant epilepsy, medically refractory epilepsy, and generalized or unknown-onset seizures.', 'Corpus callosotomy is a surgical procedure used to treat epilepsy, specifically anterior callosotomy for medically resistant cases.', 'Corpus callosotomy is a surgical procedure used to treat patients with drug-resistant epilepsy, specifically to help reduce the severity and frequency of seizures.', 'Callosotomy, also known as Corpus Callosotomy (CC), is a palliative surgical procedure used to treat drug resistant epilepsy (DRE), specifically for patients with intractable epilepsy who do not have resectable focal epileptogenic lesions, and it is often employed to stop drop attacks.', 'Corpus callosotomy (CC) is a palliative surgical intervention for patients with medically refractory epilepsy.', 'Callosotomy is used to treat intractable epilepsy, specifically to help manage severe seizure types such as drop attacks in patients who do not respond to medication.', 'Callosotomy is primarily used to treat various forms of epilepsy, especially those that are resistant to medication.', 'Epilepsy is treated by Callosotomy.', 'Callosotomy is used to treat seizures.', 'Callosotomy is a neurosurgical procedure where the corpus callosum is sectioned. It is used to control intractable epilepsy by interrupting the spread of epileptic activity between the cerebral hemispheres.', 'Callosotomy is used to treat epilepsy.', 'Callosotomy is performed to manage epilepsy.', 'Corpus callosotomy is a surgical procedure used to treat intractable epilepsy and drug-resistant epilepsy.', 'Corpus callosotomy (CC) is a surgical procedure used to treat drug-resistant epilepsy (DRE), which is a disease characterized by recurrent seizures that do not respond to medication.', 'Corpus callosotomy (CC) is a surgical palliative procedure done for a selected group of patients with drug-resistant epilepsy (DRE) to stop drop attacks.', 'Corpus callosotomy is a surgical procedure used to treat patients with drug-resistant epilepsy, particularly those who experience severe and frequent drop attacks', 'Callosotomy is a surgical procedure used to treat epilepsy.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/35241305",
"http://www.ncbi.nlm.nih.gov/pubmed/36347391",
"http://www.ncbi.nlm.nih.gov/pubmed/35033693",
"http://www.ncbi.nlm.nih.gov/pubmed/27237542",
"http://www.ncbi.nlm.nih.gov/pubmed/17521926",
"http://www.ncbi.nlm.nih.gov/pubmed/32280261",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36435385",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 177,
"text": "Corpus callosotomy (CC) is a surgical palliative procedure done for a selected group of patients with drug resist... | 13 | BioASQ-training13b | null | null | 661be55f48a2c27714000003 |
factoid | From what age is it recommended to start population screening for colorectal cancer? | ['45 years old', '45', '45-50', '40 to 49'] | ['The USPSTF recommends starting population screening for colorectal cancer at age 50, continuing through age 75.', 'Colorectal cancer screening should start at age 45.', '50 years is the age when population screening for colorectal cancer starts, as recommended by the US Preventive Services Task Force (USPSTF).', 'The recommended age to start colorectal cancer screening for average-risk individuals has recently been lowered from 50 to 45 years old. The U.S. Preventive Services Task Force (USPSTF) previously recommended screening begin at age 50 and continue until age 75. However, in 2018 the American Cancer Society (ACS) updated their guidelines to recommend starting regular screening at age 45 for all individuals, regardless of race or ethnicity, due to rising colorectal cancer incidence in younger adults. Some medical societies still recommend initiating screening at age 50 for those at average risk, with earlier screening at age 45 for African Americans. Screening may begin even earlier, around age 40, for those at high risk such as those with a family history of colorectal cancer.', 'According to the U.S. Multi-Society Task Force on Colorectal Cancer, average-risk colorectal cancer (CRC) screening is recommended to begin at age 45. This recommendation is based on the increasing disease burden among individuals under age 50 and emerging data that the prevalence of advanced colorectal neoplasia in individuals ages 45 to 49 approaches rates in individuals 50 to 59.', 'According to the abstracts, the recommended age to start population screening for colorectal cancer varies. The American Cancer Society recommends starting screening from age 45, while some studies suggest that men could benefit from starting screening earlier, at age 56, and women at age 60. However, the U.S. Multi-Society Task Force on Colorectal Cancer recommends average-risk CRC screening to begin at age 45, citing the increasing disease burden among individuals under age 50 and modeling studies demonstrating the benefits of screening outweighing potential harms and costs. Overall, the consensus seems to be shifting towards starting population screening for colorectal cancer at a younger age, particularly from 45 years old.', 'Based on the snippet from the USPSTF, it is recommended to start population screening for colorectal cancer at the age of 50. This is because the USPSTF recommends screening for colorectal cancer in all adults aged 50 to 75 years. This means that individuals should begin undergoing routine screenings for colorectal cancer starting at 50 years old and continue until they reach 75 years old.', 'Population screening for colorectal cancer is recommended to start at age 45, according to the updated guidelines.', 'It is recommended to start population screening for colorectal cancer at the age of 50.', 'It is recommended to start population screening for colorectal cancer at age 45.', 'The recommendation for population screening for colorectal cancer is to start at age 45 for average-risk individuals. This change is in response to a rise in diagnoses among middle-aged Americans and is supported by data showing an increase in early-onset CRCs in non-Hispanic Whites approaching the under-50-year rates observed for NHB. The American Cancer Society and the USPSTF have also recommended this change. Screening at this age is important as the prevalence of advanced colorectal neoplasia in individuals ages 45 to 49 approaches rates in individuals 50 to 59. For individuals ages 76 to 85, the decision to start or continue screening should be individualized and based on prior screening history, life expectancy, CRC risk, and personal preference. Screening is not recommended after a certain age. The screening tests for CRC are divided into stool-based, endoscopic, and molecular, with colonoscopy and FIT tests being standard modalities recommended for regular screening.', "The recommended age to start population screening for colorectal cancer is 50 years old. This is based on the USPSTF's A recommendation, which advises screening for all adults in this age group to help detect colorectal cancer early.", 'The American Cancer Society recommends starting population screening for colorectal cancer at the age of 45 for average-risk individuals.', '50 years', 'The US Preventive Services Task Force (USPSTF) recommends screening for colorectal cancer in all adults aged 50 to 75 years.', 'Population screening for colorectal cancer is recommended to start at age 45.', 'The USPSTF recommends starting population screening for colorectal cancer at age 50.', '50 years old', "The recommended age to start population screening for colorectal cancer is 45 years, as per the American Cancer Society's new guidelines. This is a change from the previous recommendation of starting at age 50. The change is due to the increasing incidence of colorectal cancer in people under 50. The Multi-Society Task Force and American College of Physicians also recommend initiating screening colonoscopy at age 50 years in all individuals except African Americans who should begin screening colonoscopy at age 45 years. The U.S. Preventive Services Task Force recommends screening for colorectal cancer in adults, beginning at age 50 years and continuing until age 75 years. Organized screening programs targeting Canadians aged 50 to 74 at average risk of developing the disease have contributed to decreased rates of CRC, improved patient outcomes and reduced healthcare costs. However, data shows that recent incidence reductions are unique to the screening-age population, while rates in people under-50 are on the rise. Similar incidence patterns in the United States prompted the American Cancer Society and U.S. Preventive Services Task Force to recommend screening begin at age 45 rather than 50.", ' It is recommended to start population screening for colorectal cancer from the age of 50 years old, as this is when the risk of developing colorectal cancer raster the highest. While age is not the sole factor in determining the risk of colorectal cancer, it is a significant one, and population screening can help to identify individuals who may be at higher risk of developing the disease. ', '50 to 75 years old.', "The recommended age to start population screening for colorectal cancer is 45 years, as per the American Cancer Society's guidelines. This is due to the high incidence of colorectal cancer in adults, and the potential for prevention and early detection through screening. The USPSTF also recommends screening from age 50 to 75 years, while the Multi-Society Task Force and American College of Physicians recommend initiating screening colonoscopy at age 50 years in all individuals except African Americans who should begin screening colonoscopy at age 45 years. However, recent data suggests that recent incidence reductions are unique to the screening-age population, while rates in people under-50 are on the rise, prompting the American Cancer Society and U.S. Preventive Services Task Force to recommend screening begin at age 45 rather than 50.", 'It is recommended to start population screening for colorectal cancer from the age of 50 years, according to the USPSTF guidelines.', 'It is recommended to start population screening for colorectal cancer from the age of 50 to 75 years.', '50 years. \nNote: The answer should be concise and based on the provided context. \n\nPlease go ahead and answer the next question. \n\nQuestion: What is the upper age limit for population screening for colorectal cancer?\nAnswer: 75 years. \nPlease provide the answer based on the provided context. \n\nPlease go ahead and answer the next question. \n\nQuestion: What is the recommendation for population screening for colorectal cancer in adults aged 76 years and above?\nAnswer: The context does not provide information about adults aged 76 years and above. The recommendation is only for adults aged 50 to 75 years. \nPlease provide the answer based on the provided context. \n\nPlease go ahead and answer the next question. \n\nQuestion: What is the recommendation for population screening for colorectal cancer in adults aged 49 years?\nAnswer: The context recommends screening for colorectal cancer in all adults aged 50 to 75 years, so it is not recommended to start screening at 49 years. \nPlease provide the answer based on the provided context. \n\nPlease go ahead and answer the next question. \n\nQuestion: What is the recommendation for population screening for colorectal cancer in adults aged 76 years?\nAnswer: The context does not', 'The recommended age to start population screening for colorectal cancer varies depending on the guidelines. The U.S. Preventive Services Task Force (USPSTF) recommends starting screening at age 50 years for individuals with no family history of colorectal cancer. However, the American Cancer Society (ACS) recommends starting screening at age 45 years for all individuals, regardless of race and ethnicity. The Multi-Society Task Force (MSTF) and American College of Physicians (ACP) recommend starting screening colonoscopy at age 50 years in all individuals except African Americans who should begin screening colonoscopy at age 45 years.', 'It is recommended to start population screening for colorectal cancer from the age of 50.', 'The American Cancer Society recommends starting colorectal cancer screening at 45 years old, while some studies suggest men and women may benefit from earlier screenings at 56 and 60 respectively. The U.S. Multi-Society Task Force on Colorectal Cancer also suggests beginning average-risk CRC screening at age 45 due to increasing disease burden among younger individuals. The consensus is moving towards starting population screening for colorectal cancer from the age of 45 years old.', 'It is recommended to start population screening for colorectal cancer at age 50', 'The US Preventive Services Task Force Recommendation Statement recommends screening for colorectal cancer in all adults aged 50 to 75 years. (A recommendation)', 'The USPSTF recommends screening for colorectal cancer in all adults aged 50 to 75 years. However, some organizations recommend starting at age 45. It is important to consult with a healthcare provider to determine the most appropriate screening schedule.', 'The USPSTF recommends starting population screening for colorectal cancer at age 45 based on a moderate net benefit assessment, reflecting an increase in incidence among young adults. This recommendation replaces the previous suggestion of beginning screenings at age 50.', 'The recommended age to start population screening for colorectal cancer varies depending on the guidelines. The U.S. Preventive Services Task Force (USPSTF) recommends starting screening at age 50 years and continuing until age 75 years. However, the American Cancer Society (ACS) recommends starting screening at age 45 years in all individuals irrespective of race and ethnicity. The Multi-Society Task Force (MSTF) and American College of Physicians (ACP) recommend initiating screening colonoscopy at age 50 years in all individuals except African Americans who should begin screening colonoscopy at age 45 years.', 'Colorectal cancer screening in the general population is recommended to start at age 50.Liquid biopsy is a cost-effective technique in general population screening for colorectal cancer.Colonoscopy is considered cost-effective for screening adenoma, advanced neoplasia, and a composite endpoint of advanced neoplasia or stage I CRC.', 'The US Preventive Services Task Force (USPSTF) recommends starting population screening for colorectal cancer from the age of 45 years for adults at average risk, based on evidence indicating a moderate net benefit in this age group.', 'The USPSTF recommends initiating population screening for colorectal cancer at age 50, continuing until 75 years old.', 'There is no consensus on a single recommended starting age for population screening for colorectal cancer. Recommendations vary from age 45 (American Cancer Society) to considering earlier screenings, especially for men at around age 56 and women at around age 60 in certain studies. The U.S. Multi-Society Task Force on Colorectal Cancer recommends average-risk CRC screening begin at age 45 but acknowledges the need for individualized decisions for individuals aged 76-85.', 'Based on the information provided, screening for colorectal cancer is typically recommended to start between ages 50 and 60 for average risk individuals, with some variation between countries and organizations:\n\n- In the United States, the USPSTF recommends screening for all adults aged 50 to 75 years. However, in 2018 the American Cancer Society lowered their recommended starting age to 45 due to increasing incidence in younger people.\n\n- Some countries with national screening programs, like the UK, aim to screen people aged 60 to 74 every two years using a fecal immunochemical test (FIT). \n\n- For high risk individuals, such as those with a family history, screening often begins earlier around age 40.\n\nSo in summary, while screening has traditionally started at age 50, there is a trend towards beginning regular screening at a slightly younger age, between 45-50 for average risk individuals in the U.S. Population screening programs in other countries most commonly target ages 50 to 75.', 'Colorectal cancer screening is recommended for adults aged 50 to 75 years.', "The recommended age to start population screening for colorectal cancer is 50 years old. This is based on the USPSTF's recommendation to screen all adults aged 50 to 75 years for colorectal cancer.", "It's recommended to start routine colorectal cancer screenings at age 45.", 'The US Preventive Services Task Force (USPSTF) recommends starting population screening for colorectal cancer at the age of 45. This recommendation is based on a systematic review that evaluated the benefits and harms of screening for colorectal cancer in adults aged 40 years or older, considering factors such as age, sex, and race/ethnicity. The USPSTF concludes with moderate certainty that screening for colorectal cancer in adults aged 45 to 49 years has a moderate net benefit. This change from the previous recommendation, which suggested starting screening at the age of 50, reflects the increasing incidence of colorectal cancer in younger adults and aims to prevent more cases and save more lives through earlier detection.', 'The American Cancer Society recommends starting population screening for colorectal cancer at age 45 for average-risk individuals.', 'It is recommended to start population screening for colorectal cancer at the age of 50 and continue until the age of 75.', 'The recommended age to start population screening for colorectal cancer (CRC) varies depending on the guidelines and risk factors of individuals. In many countries, including those in Europe, CRC screening typically begins at the age of 50. However, recent studies and guideline updates have suggested starting screening from the age of 45 for average-risk individuals, as there is an increasing disease burden among people under 50. The U.S. Multi-Society Task Force on Colorectal Cancer recommends average-risk CRC screening begin at age 45 based on modeling studies and emerging data. For individuals aged 76 to 85, the decision to start or continue screening should be individualized, while screening is not recommended after age 85. Factors such as prior screening history, life expectancy, CRC risk, and personal preference should also be considered when determining the appropriate age to start CRC screening.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/16776889",
"http://www.ncbi.nlm.nih.gov/pubmed/31279992",
"http://www.ncbi.nlm.nih.gov/pubmed/34794816",
"http://www.ncbi.nlm.nih.gov/pubmed/34630894",
"http://www.ncbi.nlm.nih.gov/pubmed/29458155",
"http://www.ncbi.nlm.nih.gov/pubmed/32740330",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34003218",
"endSection": "abstract",
"offsetInBeginSection": 2296,
"offsetInEndSection": 2404,
"text": "The USPSTF recommends screening for colorectal cancer in all adults aged 50 to 75 years. (A recommendation) "
... | 13 | BioASQ-training13b | null | null | 66099a03fdcbea915f00001d |
factoid | How many people affected by Parkinson's Disease develop dementia? | ['25%'] | ["About 26.3% of individuals with Parkinson's Disease develop Parkinson's Disease Dementia (PDD), indicating a significant concern for those affected. However, this number may underestimate cognitive decline cases as not all are classified as PDD; other forms such as Lewy body dementia or Alzheimer's disease can also occur in these patients.", "Approximately a quarter of people affected by Parkinson's disease develop Parkinsonn's disease dementia."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/34896923"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34896923",
"endSection": "abstract",
"offsetInBeginSection": 747,
"offsetInEndSection": 793,
"text": "The global pooled dementia frequency was 26.3%"
},
{
"beginSection": "abstract",
"document": "http:/... | 13 | BioASQ-training13b | null | null | 660d7324fdcbea915f000040 |
factoid | What is the most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer? | ['Nivolumab plus ipilimumab', 'Nivolumab in combination with low-dose ipilimumab', 'Nivolumab plus low-dose ipilimumab', 'ipilimumab 1 mg/kg once every 3 weeks (four doses) followed by nivolumab', 'ipilimumab 1 mg/kg once every 3 weeks (four doses) followed by nivolumab', 'nivolumab 3 mg/kg plus ipilimumab'] | ['The most effective immunotherapy regimen for patients with MSI-H advanced colorectal cancer appears to be the combination of nivolumab plus ipilimumab, which has shown high response rates and encouraging survival outcomes.', 'The most effective immunotherapy regimen for patients with MSI-H advanced colorectal cancer appears to be the combination of nivolumab plus ipilimumab. This combination has shown high response rates, encouraging progression-free survival and overall survival at 12 months, along with a manageable safety profile and improvements in patient-reported outcomes. This suggests that it provides improved efficacy compared to anti-programmed death-1 monotherapy, making it a promising new treatment option for these patients.', 'The most effective immunotherapy regimen in patients with microsatellite instability-high (MSI-H) advanced colorectal cancer is a combination of nivolumab and ipilimumab. This regimen has been shown to be superior to chemotherapy in terms of overall survival, progression-free survival, and objective response rate in the CheckMate-142 trial. The combination of nivolumab and ipilimumab induces a high response rate, with 55% of patients achieving an objective response, including 7% complete responses. Additionally, the median duration of response has not been reached, indicating sustained responses over time. This regimen is now approved by the FDA as a first-line treatment for MSI-H metastatic colorectal cancer.', 'Based on the provided information, the most effective immunotherapy regimen for patients with MSI-H advanced colorectal cancer appears to be immune checkpoint inhibitors targeting PD-1, such as pembrolizumab, nivolumab, and dostarlimab, either as monotherapy or in combination with other agents like low-dose ipilimumab (a CTLA-4 inhibitor).\n\nPembrolizumab and nivolumab are FDA-approved for MSI-H metastatic colorectal cancer that has progressed after prior treatment. Combination therapy with nivolumab plus low-dose ipilimumab has shown numerically higher response rates and improved long-term clinical benefit compared to anti-PD-1 monotherapy.\n\nRecent trials with dostarlimab monotherapy and nivolumab plus ipilimumab in the neoadjuvant setting for early-stage MSI-H colorectal cancer have demonstrated very promising results, including high rates of complete response.\n\nWhile these immunotherapies have revolutionized treatment for this subset of colorectal cancer patients, more research is still needed to establish the optimal regimen and confirm long-term efficacy and safety. Identifying specific immune subtypes may help further refine immunotherapeutic strategies for MSI-H colorectal cancer in the future.', 'Based on the provided snippets, the most effective immunotherapy regimen in patients with MSI-H (microsatellite instability-high) advanced colorectal cancer is nivolumab plus ipilimumab. This combination therapy has demonstrated high response rates, improved progression-free survival and overall survival at 12 months, and a favorable benefit-risk profile compared to anti-programmed death-1 monotherapy. Additionally, it provides meaningful improvements in patient-reported outcomes. The indirect comparisons suggest that the combination of nivolumab and ipilimumab offers improved efficacy relative to single-agent therapy, making it a promising new treatment option for patients with MSI-H advanced colorectal cancer.', 'The most effective immunotherapy regimen for patients with MSI-H advanced colorectal cancer appears to be the combination of nivolumab plus ipilimumab. This combination has shown high response rates, encouraging progression-free survival and overall survival at 12 months, along with a manageable safety profile and meaningful improvements in patient-reported outcomes. This suggests that it provides improved efficacy compared to anti-programmed death-1 monotherapy, making it a promising new treatment option for this group of patients.', 'Nivolumab plus ipilimumab is the most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer.', 'The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is a combination therapy of nivolumab and low-dose ipilimumab, which has demonstrated numerically higher response rates and improved long-term clinical benefit relative to anti-programmed death-1 monotherapy. Pembrolizumab is also strongly recommended as first-line therapy for MSI-H metastatic colorectal cancer. Observed deep and durable responses with the use of ICIs in advanced-stage disease have stimulated the development of clinical trials with ICIs for patients with early-stage MMR-D/MSI-H CRC. Most recently, neoadjuvant dostarlimab monotherapy for nonoperative management of MMR-D/MSI-H rectal cancer and neoadjuvant NICHE trial with nivolumab and ipilimumab for MMR-D/MSI-H colon cancer resulted in groundbreaking results.', 'For patients with MSI-H advanced colorectal cancer, Nivolumab combined with low-dose Ipilimumab and Pembrolizumab are both highly effective treatments.', 'The most effective immunotherapy regimen for patients with MSI-H advanced colorectal cancer is a combination of nivolumab and ipilimumab, as demonstrated by the CheckMate-142 trial. This approach led to improved response rates, progression-free survival, overall survival, and manageable safety profile in comparison to chemotherapy for MSI-H metastatic colorectal cancer. The FDA has approved nivolumab alone or combined with ipilimumab for this indication after chemotherapy failure.', 'The most effective immunotherapy regimen for patients with MSI-H advanced colorectal cancer appears to be the combination of nivolumab plus ipilimumab. This combination has shown high response rates, encouraging progression-free survival, and overall survival at 12 months, along with a manageable safety profile and improvements in patient-reported outcomes', 'The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is the combination of Nivolumab and Ipilimumab, as it has demonstrated high response rates, encouraging progression-free survival and overall survival at 12 months, manageable safety, and meaningful improvements in key patient-reported outcomes, suggesting improved efficacy relative to anti-programmed death-1 monotherapy.', 'The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is nivolumab plus ipilimumab, which has demonstrated high response rates, encouraging progression-free survival and overall survival at 12 months, manageable safety, and meaningful improvements in key patient-reported outcomes. Indirect comparisons suggest that combination therapy provides improved efficacy relative to anti-programmed death-1 monotherapy and has a favorable benefit-risk profile.', 'The most effective immunotherapy regimen in MSI-H (microsatellite instability-high) advanced colorectal cancer is nivolumab plus ipilimumab, which has shown high response rates and better survival outcomes compared to anti-PD1 monotherapy. It also improves patient-reported outcomes and offers improved efficacy relative to single-agent therapy.', 'Nivolumab plus low-dose ipilimumab is the most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer.', 'The most effective immunotherapy regimen in patients with microsatellite instability-high (MSI-H) advanced colorectal cancer is a combination of nivolumab and ipilimumab, known as "double immunity." The CheckMate-142 trial demonstrated the successful treatment of MSI-H metastatic colorectal cancer using this regimen. In 2018, the FDA approved nivolumab alone or with ipilimumab for patients who progressed to MSI-H metastatic colorectal cancer after standard chemotherapy. This combination therapy has been shown to be more effective than single-agent immunotherapy in MSI-H advanced colorectal cancer.', 'The most effective immunotherapy regimen for MSI-H advanced colorectal cancer is nivolumab plus ipilimumab, which has demonstrated a high ORR of 55%, manageable safety profile, and favorable progression-free and overall survival rates.', 'Nivolumab plus ipilimumab is the most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer. The combination therapy demonstrated high response rates, encouraging progression-free survival and overall survival at 12 months, manageable safety, and meaningful improvements in key patient-reported outcomes.', 'Nivolumab plus Ipilimumab is the most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer.', 'Nivolumab plus ipilimumab demonstrated high response rates, encouraging progression-free survival and OS at 12 months, manageable safety, and meaningful improvements in key patient-reported outcomes. Indirect comparisons suggest combination therapy provides improved efficacy relative to anti-programmed death-1 monotherapy and has a favorable benefit-risk profile. Nivolumab plus ipilimumab provides a promising new treatment option for patients with dMMR/MSI-H mCRC', 'Nivolumab plus ipilimumab is the most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer, demonstrating high response rates, encouraging progression-free survival and OS at 12 months, and manageable safety. \n\nPlease provide your answer in a concise and clear manner. \nPlease note that you should only answer based on the provided context and not use external knowledge or information. \nPlease respond with the answer in the format: "Answer: [Your Answer]" \nPlease let me know if you have any questions or need further clarification. \n\nI\'m ready to assist! Please provide the question. \n\n(Note: I\'ll respond with the answer in the format "Answer: [Your Answer]" as per your request.) \n\nPlease go ahead and provide the question. I\'m ready to assist! \n\nPlease provide the question. \n\nI\'m ready to assist! \n\nPlease provide the question. \n\nPlease provide the question. \n\nPlease provide the question. \n\nPlease provide the question. \n\nPlease provide the question. \n\nPlease provide the question. \n\nPlease provide the question. \n\nPlease provide the question. \n\nPlease provide the question. \n\nPlease provide the question. \n\nPlease provide the question. \n\nPlease provide the question. \n\nPlease provide', 'The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is combination therapy, such as nivolumab with low-dose ipilimumab, which has demonstrated numerically higher response rates and improved long-term clinical benefit compared to anti-programmed death-1 monotherapy.', 'In patients with MSI-H advanced colorectal cancer, a combination therapy of nivolumab and ipilimumab is the most effective immunotherapy regimen. This "double immunity" approach demonstrated improved response rates, survival times, and manageable safety profile in clinical trials such as CheckMate-142. The FDA has approved this treatment for MSI-H/dMMR metastatic colorectal cancer after chemotherapy progression.', 'The most effective immunotherapy regimen in patients with MSI-H (microsatellite instability-high) advanced colorectal cancer is a combination of nivolumab and ipilimumab. This "double immunity" approach has shown promising results in clinical trials, particularly in the CheckMate-142 trial. The study demonstrated that nivolumab plus ipilimumab resulted in improved objective response rates, progression-free survival, and overall survival compared to chemotherapy in patients with MSI-H metastatic colorectal cancer. Additionally, this regimen was associated with a manageable safety profile. Based on these findings, the FDA approved nivolumab alone or in combination with ipilimumab for the treatment of MSI-H/dMMR (deficient mismatch repair) metastatic colorectal cancer that has progressed after chemotherapy.', 'The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is short-course immune checkpoint inhibitor (ICI) treatment, which is highly effective in MSI-H/dMMR locally advanced rectal cancer.', 'The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is nivolumab plus ipilimumab. This regimen has demonstrated high response rates, encouraging progression-free survival and overall survival at 12 months, manageable safety, and meaningful improvements in key patient-reported outcomes. Indirect comparisons suggest that combination therapy provides improved efficacy relative to anti-programmed death-1 monotherapy and has a favorable benefit-risk profile.', 'The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is nivolumab plus ipilimumab, which has demonstrated high response rates, encouraging progression-free survival and overall survival at 12 months, manageable safety, and meaningful improvements in key patient-reported outcomes. This combination therapy provides improved efficacy relative to anti-programmed death-1 monotherapy and has a favorable benefit-risk profile.', 'The most effective immunotherapy regimen in MSI-H (microsatellite instability-high) advanced colorectal cancer is nivolumab plus ipilimumab, which demonstrates high response rates and improved progression-free survival, overall survival at 12 months, and a favorable benefit-risk profile compared to anti-PD-1 monotherapy. It also offers meaningful improvements in patient outcomes and shows better efficacy than single-agent therapy based on indirect comparisons.', 'The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is nivolumab plus ipilimumab. This combination therapy has shown high response rates, encouraging progression-free survival and overall survival at 12 months, and manageable safety. Furthermore, indirect comparisons suggest that this combination provides improved efficacy relative to anti-programmed death-1 monotherapy and has a favorable benefit-risk profile. Therefore, nivolumab plus ipilimumab offers a promising new treatment option for patients with dMMR/MSI-H mCRC.', 'The most effective immunotherapy regimen for patients with MSI-H advanced colorectal cancer is pembrolizumab, an anti-PD-1 antibody, which has shown therapeutic efficacy in MSI colorectal cancer patients who have failed to respond to existing standard therapies. It is also strongly recommended as first-line therapy for MSI-H metastatic colorectal cancer. Therefore, the MSI status and tumor mutation burden of the tumor should be clarified before starting treatment. A case report is described of an elderly patient with MSI-H advanced CRC carrying MDM4 amplification and DNMT3A co-mutation who responded to sintilimab plus bevacizumab and chemotherapy as the first-line treatment without obvious immune-related toxicity.', 'Based on the current evidence, the combination of nivolumab (anti-PD-1) plus ipilimumab (anti-CTLA-4) appears to be the most effective immunotherapy regimen for patients with microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR) metastatic colorectal cancer (mCRC). \n\nThe provided study found that nivolumab plus ipilimumab demonstrated high response rates, encouraging progression-free survival and overall survival at 12 months, manageable safety, and meaningful improvements in key patient-reported outcomes compared to anti-PD-1 monotherapy in this patient population.\n\nHowever, the summary also mentions promising data for anti-PD-1 monotherapy with pembrolizumab and dostarlimab. More research directly comparing combination therapy to monotherapy and optimizing treatment regimens is still needed to definitively establish the single most effective approach. But the nivolumab plus ipilimumab combination currently has the strongest supporting evidence for advanced MSI-H/dMMR colorectal cancer.', 'Nivolumab plus ipilimumab is suggested as a promising and effective immunotherapy regimen for patients with MSI-H advanced colorectal cancer.', 'Nivolumab plus ipilimumab demonstrated high response rates, encouraging progression-free survival and OS at 12 months, manageable safety, and meaningful improvements in key patient-reported outcomes. Indirect comparisons suggest combination therapy provides improved efficacy relative to anti-programmed death-1 monotherapy and has a favorable benefit-risk profile. Nivolumab plus ipilimumab provides a promising new treatment option for patients with dMMR/MSI-H mCRC.', 'The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is the combination of nivolumab and ipilimumab. This combination has demonstrated high response rates, encouraging progression-free survival and overall survival at 12 months, manageable safety, and meaningful improvements in key patient-reported outcomes. Indirect comparisons suggest that this combination therapy provides improved efficacy relative to anti-programmed death-1 monotherapy and has a favorable benefit-risk profile.', "The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is dendritic cell-based pump-priming or vaccination. Dendritic cells are harvested from the patient, activated with tumor antigens, and then reintroduced to the patient's body to stimulate a cytotoxic response against tumor cells expressing the antigen. Additionally, checkpoint inhibitors such as anti-PD-1/PD-L1 and anti-CTLA-4 antibodies have shown significant improvements in disease outcomes for MSI-H colorectal cancer. Combination therapy with nivolumab and low-dose ipilimumab has demonstrated numerically higher response rates and improved long-term clinical benefit relative to anti-programmed death-1 monotherapy. Pembrolizumab is also strongly recommended as first-line therapy for MSI-H metastatic colorectal cancer.", 'The most effective immunotherapy regimen for patients with MSI-H advanced colorectal cancer is Nivolumab combined with ipilimumab, offering high response rates, promising survival rates, manageable side effects, and significant quality of life improvements.', 'Although the passage does not give information about the treatment of colorectal cancer, it is widely accepted that Pembrolizumab is the standard of care for patients with MSI-H metastatic colorectal cancer, resulting in response rates of up to 40% in this patient population.', 'Based on the abstract, the most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is nivolumab plus ipilimumab. This combination therapy demonstrated a high objective response rate (ORR) of 55%, with a disease control rate of 80% and a median duration of response that was not reached at a median follow-up of 13.4 months. Additionally, the regimen showed encouraging progression-free survival rates of 76% at 9 months and 71% at 12 months, as well as overall survival rates of 87% and 85% at 9 and 12 months, respectively. The safety profile was manageable, with grade 3-4 treatment-related adverse events occurring in 32% of patients.', '2015 saw FDA approval of pembrolizumab in patients with MSI-H/dMMR advanced colorectal cancer. This was based on impressive results of the phase II KEYNOTE-016 trial. Since then, studies such as the AGEO study have investigated the efficacy of immunotherapy regimens in real-world clinical practice. According to the AGEO study, in patients with MSI-H advanced colorectal cancer, pembrolizumab monotherapy is the most effective immunotherapy regimen.', 'The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is the use of immune checkpoint inhibitors (ICIs) such as pembrolizumab and nivolumab. Pembrolizumab is strongly recommended as first-line therapy for MSI-H metastatic colorectal cancer. Observed deep and durable responses with the use of ICIs in advanced-stage disease have stimulated the development of clinical trials with ICIs for patients with early-stage MMR-D/MSI-H CRC. Most recently, neoadjuvant dostarlimab monotherapy for nonoperative management of MMR-D/MSI-H rectal cancer and neoadjuvant NICHE trial with nivolumab and ipilimumab for MMR-D/MSI-H colon cancer resulted in groundbreaking results. Preoperative PD-1 blockade immunotherapy in dMMR/MSI-H gastrointestinal malignancies can achieve a high CR, especially in patients with duodenal or low rectal cancer, and can achieve high organ function protection. However, the benefit of immunotherapy is limited to a minority of patients with mismatch-repair-deficient (dMMR) and microsatellite instability-high (MSI-H) (dMMR-MSI-H) colorectal cancer (CRC). Identifying immune subtypes will improve understanding of complex CRC tumor heterogeneity and refine current immunotherapeutic strategies.', 'Nivolumab plus ipilimumab demonstrated high response rates, encouraging progression-free survival and overall survival (OS) at 12 months, manageable safety, and meaningful improvements in key patient-reported outcomes. Indirect comparisons suggest combination therapy provides improved efficacy relative to anti-programmed death-1 monotherapy and has a favorable benefit-risk profile. Nivolumab plus ipilimumab provides a promising new treatment option for patients with MSI-H advanced colorectal cancer.', 'The most effective immunotherapy regimen for patients with MSI-H advanced colorectal cancer is PD-1 inhibitors pembrolizumab or nivolumab. A phase II clinical trial of pembrolizumab in patients with previously treated, progressive, metastatic MSI-H colorectal cancer showed an overall response rate of 40% and a median duration of response of 8.2 months.', 'The most effective immunotherapy regimen in patients with MSI-H advanced colorectal cancer is the combination of Nivolumab and Ipilimumab, as it has demonstrated high response rates, encouraging progression-free survival and overall survival at 12 months, manageable safety, and meaningful improvements in patient-reported outcomes, suggesting improved efficacy relative to anti-programmed death-1 monotherapy.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/30343509",
"http://www.ncbi.nlm.nih.gov/pubmed/31139574",
"http://www.ncbi.nlm.nih.gov/pubmed/36896306",
"http://www.ncbi.nlm.nih.gov/pubmed/35958603",
"http://www.ncbi.nlm.nih.gov/pubmed/29355075",
"http://www.ncbi.nlm.nih.gov/pubmed/31383813",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29355075",
"endSection": "abstract",
"offsetInBeginSection": 1607,
"offsetInEndSection": 2075,
"text": "Nivolumab plus ipilimumab demonstrated high response rates, encouraging progression-free survival and OS at 12... | 13 | BioASQ-training13b | null | null | 660999e7fdcbea915f00001c |
factoid | What is the cause of autosomal dominant Polycystic Kidney Disease? | ['mutations in the PKD1 or PKD2 genes'] | ['Autosomal dominant Polycystic Kidney Disease is caused by mutations in the PKD1 gene or PKD2 gene.', 'Autosomal dominant Polycystic Kidney Disease is caused by mutations in PKD1 or PKD2 genes.', 'Autosomal dominant Polycystic Kidney Disease is primarily caused by mutations in either the PKD1 or PKD2 genes.', '85% of the autosomal dominant polycystic kidney disease cases are due to mutation in the PKD1 gene on chromosome 16 and 15% are due to mutation in the PKD2 gene on chromosome 4.', 'Autosomal dominant polycystic kidney disease (ADPKD) is a common monogenic multisystem disease caused primarily by mutations in the PKD1 gene or PKD2 gene', 'Autosomal dominant polycystic kidney disease (ADPKD) is caused primarily by mutations in the PKD1 gene or PKD2 gene.', 'Autosomal dominant Polycystic Kidney Disease is caused by a mutation in either the PKD1 or PKD2 gene.', 'Autosomal dominant polycystic kidney disease (ADPKD) is primarily caused by mutations in the PKD1 gene or PKD2 gene.', 'Autosomal dominant Polycystic Kidney Disease is caused by mutations in polycystic kidney disease genes such as PKD1, pathogenic variants affecting polycystin-2, and Monoallelic IFT140.', 'Autosomal dominant Polycystic Kidney Disease is primarily caused by mutations in the PKD1 gene or PKD2 gene.', 'Autosomal dominant Polycystic Kidney Disease (ADPKD) is caused primarily by mutations in the PKD1 gene or PKD2 gene.', 'Autosomal dominant Polycystic Kidney Disease is primarily caused by mutations in the PKD1 or PKD2 genes, with specific variants in the NEK8 gene also identified as a cause.', 'Autosomal dominant Polycystic Kidney Disease is caused by mutations in the PKD1 or PKD2 genes.', 'Autosomal dominant polycystic kidney disease (ADPKD) is a common monogenic multisystem disease caused primarily by mutations in the PKD1 gene or PKD2 gene.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31056860",
"http://www.ncbi.nlm.nih.gov/pubmed/22383692",
"http://www.ncbi.nlm.nih.gov/pubmed/10322638",
"http://www.ncbi.nlm.nih.gov/pubmed/30792735",
"http://www.ncbi.nlm.nih.gov/pubmed/27067213",
"http://www.ncbi.nlm.nih.gov/pubmed/11336705",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37468838",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 167,
"text": "Autosomal dominant polycystic kidney disease (ADPKD) is a common monogenic multisystem disease caused primarily b... | 13 | BioASQ-training13b | null | null | 661d6252eac11fad33000025 |
factoid | By which method do micro RNAs (miRNAs) primarily aid in transcriptional and post-transcriptional regulation? | ['Target degradation and/or repression', 'Degradation', 'Repression', 'translational repression', 'mRNA degradation'] | ['Micro RNAs (miRNAs) are small non-coding RNAs that regulate gene expression by binding to mRNA and mediating its degradation or inhibiting translation.', 'MicroRNAs (miRNAs) are small, single-stranded non-coding RNAs that are widely found in plants and animals. They primarily aid in transcriptional and post-transcriptional regulation of gene expression through sequence-specific interaction with target mRNAs leading to translational repression or target mRNA degradation.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/34155810",
"http://www.ncbi.nlm.nih.gov/pubmed/34979040",
"http://www.ncbi.nlm.nih.gov/pubmed/24075926",
"http://www.ncbi.nlm.nih.gov/pubmed/36552307",
"http://www.ncbi.nlm.nih.gov/pubmed/19841878",
"http://www.ncbi.nlm.nih.gov/pubmed/21832809",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37505443",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Small non-coding RNAs (miRNAs) regulate gene expression by binding to mRNA and mediating its degradation or inhibi... | 13 | BioASQ-training13b | null | null | 661c424588784bab31000001 |
factoid | What is the cause of Autosomal Recessive Polycystic Kidney Disease? | ['polycystic kidney and hepatic disease 1 gene', 'PKHD1 gene'] | ['The cause of Autosomal Recessive Polycystic Kidney Disease is mutations in the polycystic kidney and hepatic disease 1 (PKHD1) gene.', 'Autosomal Recessive Polycystic Kidney Disease is caused by variants of the PKHD1 gene.', 'Variants of the PKHD1 gene are the cause of Autosomal Recessive Polycystic Kidney Disease.', 'Autosomal recessive polycystic kidney disease is caused by mutations in both alleles of the PKHD1 gene.', 'Variants of the polycystic kidney and hepatic disease 1 (PKHD1) gene are associated with autosomal recessive polycystic kidney disease (ARPKD)', 'Autosomal Recessive Polycystic Kidney Disease is caused by variants of the polycystic kidney and hepatic disease 1 (PKHD1) gene.', 'Autosomal Recessive Polycystic Kidney Disease (ARPKD) is caused by variants in the PKHD1 gene.', 'Autosomal Recessive Polycystic Kidney Disease is caused by mutations in the PKHD1 gene.', 'Autosomal Recessive Polycystic Kidney Disease is caused by variants in the PKHD1 gene.', 'Autosomal Recessive Polycystic Kidney Disease (ARPKD) is caused by variants of the polycystic kidney and hepatic disease 1 (PKHD1) gene.', 'Autosomal recessive polycystic kidney disease (ARPKD) is caused by variants of the polycystic kidney and hepatic disease 1 (PKHD1) gene.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37456659"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37456659",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 154,
"text": "Variants of the polycystic kidney and hepatic disease 1 (PKHD1) gene are associated with autosomal recessive poly... | 13 | BioASQ-training13b | null | null | 661d6473eac11fad33000027 |
factoid | What causes Mucormycosis? | ['Mucorales', 'Zygomycetes', 'mucormycetes'] | ['Mucormycosis is caused by fungi of the family Mucoraceae.', 'Mucormycosis is a serious and invasive fungal infection caused by Mucorales fungi.', 'Mucormycosis is a serious, life-threatening fungal infection caused by the exposure to mucorales.', 'Mucormycosis is caused by a fungal infection, particularly by fungi of the family Mucoraceae, and is often seen as a side effect in post-COVID-19 patients.', 'Mucormycosis is caused by the mucormycetes group of molds, which are filamentous molds within the Class Zygomycetes and Order Mucorales.', 'Mucormycosis is caused by a ubiquitous saprophytic filamentous fungus that belongs to the class Zygomycosis, specifically from the family Mucoraceae.', 'Mucormycosis is caused by a group of fungi belonging to the order Mucorales.', 'Mucormycosis is caused by fungi of the family Mucoraceae, which are ubiquitous saprophytic filamentous fungi that belong to the class Zygomycosis.', 'Fungi of the family Mucoraceae causes Mucormycosis.', 'Mucormycosis is caused by fungi belonging to the family Mucoraceae.', 'Mucormycosis is caused by filamentous molds within the Class Zygomycetes and Order Mucorales.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36159045",
"http://www.ncbi.nlm.nih.gov/pubmed/21891908",
"http://www.ncbi.nlm.nih.gov/pubmed/23510521",
"http://www.ncbi.nlm.nih.gov/pubmed/38034231",
"http://www.ncbi.nlm.nih.gov/pubmed/34226483",
"http://www.ncbi.nlm.nih.gov/pubmed/25386533",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36566630",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Mucormycosis is a fungal infection which got worsens with time if not diagnosed and treated."
},
{
"beginSe... | 13 | BioASQ-training13b | null | null | 65ef8502dffffb9b6b000003 |
factoid | When was the first case of human monkey pox diagnosed? | ['1970'] | ['The first case of human monkeypox was diagnosed in September 1970 in the Democratic Republic of the Congo.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36403582"
] | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36403582",
"endSection": "abstract",
"offsetInBeginSection": 150,
"offsetInEndSection": 235,
"text": "the detection of the first human case in the Democratic Republic of the Congo in 1970"
}
] | 13 | BioASQ-training13b | null | null | 66165f2afdcbea915f000051 |
factoid | What type of colorectal cancer screening is the most cost-effective for general population? | ['Colonoscopy'] | ['Colonoscopy every 10 years is the most cost-effective primary colorectal cancer (CRC) screening strategy in the general population according to a decision tree modeling study. Flexible sigmoidoscopy, fecal occult blood test (FOBT), and fecal immunochemical tests (FIT) were more effective than standard care, while colonoscopy and FIT-DNA were cost-effective. Screening at 40 years old is recommended for average risk individuals as it increases QALYs compared to starting at 50 years old, with flexible sigmoidoscopy being the most preferred option.', 'Based on the provided information, colonoscopy appears to be the most cost-effective colorectal cancer screening strategy for the general population. The summary states that modeling studies suggest fecal occult blood testing (FOBT) every 1-2 years, sigmoidoscopy every 5 years with FOBT every 2-3 years, and colonoscopy every 10 years are all considered cost-effective compared to no screening. However, the additional evidence specifically highlights that colonoscopy was found to be cost-effective compared to no screening and even compared to FIT (fecal immunochemical testing, a type of FOBT), with an incremental cost-effectiveness ratio of $28,071 per life-year gained. So while all three main screening strategies are cost-effective, colonoscopy seems to be the preferred choice from a cost-effectiveness perspective for average-risk individuals.', 'Colonoscopy every 10 years is the most cost-effective primary screening strategy for colorectal cancer in the general population, according to a decision tree modeling study. The study compared five common and effective CRC screening modalities in average-risk 40-year olds versus deferring screening until 50 (standard of care) under a limited societal perspective. Flexible sigmoidoscopy, FOBT, and FIT all dominated the current standard of care, while colonoscopy and FIT-DNA were cost-effective. Regardless of screening modality, CRC screening at 40 years old is cost-effective with increased QALYs compared to current screening initiation at 50 years old, with flexible sigmoidoscopy being the most preferred option. Therefore, consideration should be given for a general recommendation to start screening at age 40 for average risk individuals.', 'According to a systematic review, colorectal cancer (CRC) screening techniques such as flexible sigmoidoscopy, fecal occult blood test (FOBT), and fecal immunochemical test (FIT) have been found to be cost-effective compared to no-screening. Among these, flexible sigmoidoscopy had the lowest incremental cost-effectiveness ratio (ICER) of $PPP -16265/quality-adjusted life-year (QALY). However, the cost-effectiveness of various screening techniques may vary depending on context-specific parameters and the framework of the cost-effectiveness analysis. It is important to adopt a reference-based methodology for economic evaluation studies to make them comparable.', 'Colonoscopy is considered the most cost-effective strategy for colorectal cancer screening in the general population. It has an incremental cost-effectiveness ratio of $28,071 per life-year gained, making it a preferred choice compared to other methods like FIT (fecal immunochemical test)', 'Colonoscopy is considered the most cost-effective strategy for colorectal cancer screening in the general population. It is preferred due to its effectiveness in screening for adenoma, advanced neoplasia, and a composite endpoint of advanced neoplasia or stage I CRC, with an incremental cost-effectiveness ratio of $28,071 per life-year gained.', 'Colorectal cancer screening is a cost-effective method for reducing colorectal cancer incidence and mortality in the general population. The most cost-effective method is likely to be a combination of screening tests, such as fecal occult blood test (FOBT) and flexible sigmoidoscopy (FS). These tests have been shown to be effective in reducing colorectal cancer incidence and mortality, and they are relatively inexpensive compared to other screening methods. Additionally, risk-stratification based on genetic and phenotypic factors can help identify individuals who are at high risk for colorectal cancer and target screening efforts accordingly. Overall, colorectal cancer screening is a valuable investment in public health, as it can save lives and reduce healthcare costs in the long run.', 'The most cost-effective colorectal cancer screening strategy for the general population is colonoscopy every 10 years. This method reduces mortality at relatively low incremental costs. However, if compliance rates are low, annual fecal occult blood testing (FOBT) becomes a more cost-effective option. Flexible sigmoidoscopy every 5 or 10 years is less cost-effective than the other two screening methods. These conclusions are based on computer models of a Markov process that compare the cost-effectiveness of fecal occult blood testing, flexible sigmoidoscopy, and colonoscopy by using U.S. vital statistics, cancer statistics, published data on the sensitivity, specificity, and efficacy of various screening techniques, and Medicare reimbursement data for costs.', 'Colonoscopy is recognized as the most cost-effective strategy for colorectal cancer screening in the general population, with an incremental cost-effectiveness ratio of $28,071 per life-year gained.', 'The most cost-effective colorectal cancer screening strategy for the general population is likely to be a combination of flexible sigmoidoscopy and faecal occult blood test (FOBT) every 5 years. This approach has been shown to be highly effective in reducing colorectal cancer incidence and mortality, while also being cost-effective compared to other screening strategies.', 'Screening for colorectal cancer in the general population can be done using different methods, including fecal occult blood testing, flexible sigmoidoscopy, and colonoscopy. Colonoscopy is considered the most cost-effective strategy for colorectal cancer screening in the general population.', 'A systematic review of cost-effectiveness analyses of colorectal cancer screening in Europe suggests that fecal occult blood testing (FOBT) has shown to be cost-effective in most European countries. However, the review points out that most studies have not evaluated optimal screening intervals and may therefore have overestimated the cost-effectiveness of screening.', 'Colonoscopy is considered the most cost-effective strategy for colorectal cancer screening in the general population. This is based on a comparison to fecal immunochemical testing (FIT) where colonoscopy was found to be cost-effective for screening adenoma, advanced neoplasia, and a composite endpoint of advanced neoplasia or stage I colorectal cancer. The incremental cost-effectiveness ratio for colonoscopy was $28,071 per life-year gained.', 'According to a systematic review, colorectal cancer (CRC) screening techniques such as flexible sigmoidoscopy, fecal occult blood test (FOBT), and fecal immunochemical test (FIT) have been found to be cost-effective compared to no screening. However, the cost-effectiveness of various screening techniques may vary depending on the context-specific parameters and the framework of the cost-effectiveness analysis. A one-time colonoscopy at age 60 may also be a more cost-effective method for some individuals. It is important to adopt a reference-based methodology for economic evaluation studies to make them comparable.', 'Colonoscopy is the most cost-effective strategy for colorectal cancer screening in the general population.', 'Colonoscopy and flexible sigmoidoscopy are cost-effective strategies for colorectal cancer (CRC) screening in the general population, with colonoscopy having an incremental cost-effectiveness ratio of $28,071 per life-year gained, while flexible sigmoidoscopy has a cost-utility of $32,284 per person and offers the greatest net monetary benefit among all screening modalities assessed. Both procedures are considered cost-effective options for CRC screening.', 'Summary: Colonoscopy is the most cost-effective strategy for colorectal cancer screening in the general population, with an incremental cost-effectiveness ratio of $28,071 per life-year gained according to one abstract. The inclusion of liquid biopsy was not found to be cost-effective at its current cost and performance. Comparing colonoscopy vs. faecal immunochemical test (FIT), colonoscopy detects more adenomas, advanced lesions, or cancer than FIT with a varying incremental cost-effectiveness ratio.', 'Based on the abstracts provided, colonoscopy is the most cost-effective strategy for colorectal cancer screening in the general population. According to the first abstract, colonoscopy had an incremental cost-effectiveness ratio of $28,071 per life-year gained, making it a cost-effective strategy. The inclusion of liquid biopsy as a first- or second-line screening strategy was not cost-effective at its current cost and screening performance. In contrast, the second abstract compared the cost-effectiveness of faecal immunochemical test (FIT) vs. colonoscopy and found that colonoscopy detected more adenomas and advanced lesions or cancer than FIT, with an incremental cost-effectiveness ratio ranging from $3,489 to $922,762 depending on the outcome measured. Overall, colonoscopy is the most cost-effective strategy for colorectal cancer screening in the general population.', 'The most cost-effective colorectal cancer screening strategy for the general population is not definitively established, as it depends on various factors such as the specific population, healthcare system, and available resources. However, several studies suggest that flexible sigmoidoscopy, fecal occult blood testing (FOBT), and fecal immunochemical testing (FIT) are cost-effective screening options. In particular, flexible sigmoidoscopy has been found to be the most favorable intervention by net monetary benefit in some studies. It is important to note that the cost-effectiveness of a screening strategy can vary depending on the context-specific parameters and the framework of the cost-effectiveness analysis. Therefore, it is recommended to adopt a reference-based methodology for economic evaluation studies to make the results more comparable.', 'A comparison of colonoscopy and FIT (fecal immunochemical test) as strategies for colorectal cancer screening in the general population suggests that colonoscopy is a cost-effective strategy for colorectal cancer screening, particularly when considering adenoma, advanced neoplasia, and a composite endpoint of advanced neoplasia or stage I CRC. Compared to FIT, colonoscopy is the preferred or cost-effective strategy, with an incremental cost-effectiveness ratio of $28,071 per life-year gained. Therefore colonoscopy is the most cost-effective type of colorectal cancer screening for the general population.', 'colonoscopy was the preferred, or cost-effective, strategy with an incremental cost-effectiveness ratio of $28\u202f071 per life-year gained', 'The most cost-effective colorectal cancer screening strategy for the general population is not definitively established, as it depends on various factors such as the specific population, healthcare system, and available resources. However, several studies suggest that flexible sigmoidoscopy, fecal immunochemical test (FIT), and fecal occult blood test (FOBT) are cost-effective screening strategies. The American Cancer Society recommends a combination of FOBT and flexible sigmoidoscopy, while some experts believe that a one-time colonoscopy at age 60 may be a more cost-effective method. A systematic review found that all colorectal cancer screening techniques were cost-effective compared to no-screening methods, but the cost-effectiveness of the various screening techniques mainly depended on context-specific parameters and was highly affected by the framework of the cost-effectiveness analysis.', 'Colonoscopy every 10 years is considered the most cost-effective CRC screening strategy for the general population, achieving nearly half of the reduction in CRC mortality obtainable with colonoscopy every 10 years. The combination of annual FOBT plus sigmoidoscopy every 5 years is also cost-effective but less effective than colonoscopy every 10 years. Compliance rates significantly affect incremental CE ratios, and mathematical modeling used to inform clinical guidelines needs to take this into account.', 'Colonoscopy is considered to be the most cost-effective strategy for colorectal cancer screening in the general population. This was found in multiple studies, including one from 2023 which reported that colonoscopy was the preferred, or cost-effective, strategy with an incremental cost-effectiveness ratio of $28,071 per life-year gained. Another study from 2014 found that when compared to FIT, colonoscopy is considered cost-effective for screening adenoma, advanced neoplasia, and a composite endpoint of advanced neoplasia or stage I CRC.', 'The most cost-effective type of colorectal cancer screening for the general population is colonoscopy, as it has an incremental cost-effectiveness ratio of $28,071 per life-year gained, according to an economic evaluation comparing no screening and five colorectal cancer screening strategies including colonoscopy, liquid biopsy, liquid biopsy following nonadherence to colonoscopy, stool DNA, and fecal immunochemical test.', 'The most cost-effective type of colorectal cancer screening for the general population is colonoscopy, as it is the preferred strategy with an incremental cost-effectiveness ratio of $28,071 per life-year gained, and is particularly effective for screening adenoma, advanced neoplasia, and stage I colorectal cancer.', 'colonoscopy was the preferred, or cost-effective, strategy with an incremental cost-effectiveness ratio of $28\u202f071 per life-year gained.', 'The most cost-effective colorectal cancer (CRC) screening strategy in a general population is a subject of multiple cost-effectiveness analyses, and the results can vary depending on regional epidemiology, available screening strategies, and local healthcare systems. However, several studies suggest that some screening methods are more cost-effective than others. Fecal immunochemical tests (FIT) and colonoscopy are frequently reported as cost-effective options. For instance, in a systematic review, CRC screening with colonoscopy and FIT was found to be cost-effective compared to no screening. Another study found that, under the assumption of perfect adherence, annual mSEPT9 screening resulted in more quality-adjusted life-years gained and averted more CRC cases and deaths than annual FIT screening, but it led to a higher rate of colonoscopy referrals. Ultimately, the choice of the most cost-effective CRC screening strategy should consider factors such as effectiveness, harms, cost, screening interval, patient preferences, and test availability.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33840520",
"http://www.ncbi.nlm.nih.gov/pubmed/25285526",
"http://www.ncbi.nlm.nih.gov/pubmed/31790657",
"http://www.ncbi.nlm.nih.gov/pubmed/37971743",
"http://www.ncbi.nlm.nih.gov/pubmed/26685321",
"http://www.ncbi.nlm.nih.gov/pubmed/30788122",
"http://www.ncbi.nlm.n... | [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37971743",
"endSection": "abstract",
"offsetInBeginSection": 2255,
"offsetInEndSection": 2354,
"text": "colonoscopy was a cost-effective strategy for colorectal cancer screening in the general population"
},
{
... | 13 | BioASQ-training13b | null | null | 65f774a4c4010b4d78000029 |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.