PMCID string | Title string | Sentences string |
|---|---|---|
PMC10669128 | Preclinical Models of Visceral Sarcomas | In particular, xenografts, such as mice injected with subcutaneous cell lines or PDXs, are commonly employed for STS studies. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | For this purpose, immunocompromised mice are the most used models, although they might select for clones that do not fully represent the human neoplasm. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | Xenografts have the advantage of allowing rapid compound efficacy screening and precise in vitro cell manipulation (e.g., gene overexpression or knock-down). |
PMC10669128 | Preclinical Models of Visceral Sarcomas | They can also produce a large number of tumors which can be isolated and analyzed. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | Nonetheless, the most relevant drawback of xenografts is the lack of a reliable model of human tumor cell and mouse stroma interactions. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | Another major issue is the fact that the animals are immunocompromised, hindering the immune system’s role in tumor growth, progression, metastasis, and response to therapy . |
PMC10669128 | Preclinical Models of Visceral Sarcomas | On the contrary, in a genetically engineered mouse, tumors arise in an authentic cancer microenvironment and, more importantly, the animal’s immune system remains intact . |
PMC10669128 | Preclinical Models of Visceral Sarcomas | Thus, compared to xenografts, GEMMs allow for a better replication of the interactions between tumor cells and the host microenvironment, allowing us to test mutation effects in a physiological context. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | However, to generate and maintain GEM mice is expensive which, added to the complexity of results interpretation, leads to critical limitations . |
PMC10669128 | Preclinical Models of Visceral Sarcomas | In the field of sarcoma research, non-murine models, such as genetically modified zebrafish, have also been developed, but they primarily concern rhabdomyosarcomas, Ewing’s sarcoma, malignant peripheral nerve sheath tumors, chordomas , and, to the best of our knowledge, only one liposarcoma case . |
PMC10669128 | Preclinical Models of Visceral Sarcomas | Visceral sarcomas are generally investigated after the completion of the transformation process. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | Hence, there is a compelling need to establish robust preclinical models that can faithfully replicate sarcomagenesis in vitro and in vivo. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | Simultaneously, the need to discover new potential targets for personalized therapies is increasingly relevant. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | This requires the establishment of reliable and predictive sarcoma models of patient response, to test only the most promising therapeutic approaches in clinical trials. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | Future research should define the specific phenotype of cancer cells at the origin of different sarcoma histotypes and elucidate the mechanisms driving their transformation. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | In this regard, a valuable research tool is represented by induced pluripotent stem cells. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | This model has already been effectively applied in the field of genetic and oncological diseases, thanks to its capability to reproduce disease phenotypes within the appropriate cellular lineage . |
PMC10669128 | Preclinical Models of Visceral Sarcomas | The ability to derive tissue-specific isogenic iPSC lines, modified via genome editing at the level of driver oncogenes, would allow us to mimic different sarcoma subtypes in vitro. |
PMC10669128 | Preclinical Models of Visceral Sarcomas | iPSCs, along with three-dimensional cellular systems, might overcome the issues associated with the use of animal models and the limitations of the 2D cultures discussed in this review. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | •Enhanced glycolysis in GIST is an important metabolic feature.•GLUT play a significant role in GIST progression and response to treatment.•Glycolysis can lead to the therapeutic strategies for GIST. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Enhanced glycolysis in GIST is an important metabolic feature. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | GLUT play a significant role in GIST progression and response to treatment. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Glycolysis can lead to the therapeutic strategies for GIST.Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the digestive tract . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | GIST primarily develops due to the constitutive activation of the receptor tyrosine kinase KIT or PDGFRA, with approximately 75 % of GISTs harboring gain-of-function mutations in KIT . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Surgical resection is the primary treatment option for GISTs that can be removed. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | However, for GISTs that are unresectable, metastatic, or recurrent, KIT inhibitors, such as imatinib mesylate (also known as imatinib), are administered [, , ]. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Drug resistance represents a major obstacle to the treatment of GISTs. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Typically, resistance to imatinib develops after a median duration of 18–24 months of therapy . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | While sunitinib and regorafenib are considered effective for treating imatinib-resistant GIST, the median progression-free survival is 8.5 months for sunitinib and 4.8 months for regorafenib [, , ]. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | A recent study has highlighted the potential of TAS-116, a heat shock protein 90 inhibitor, in the treatment of treatment-resistant advanced GISTs . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Nonetheless, only a few chemotherapy regimens are available for GIST, and no chemotherapy regimens are available for imatinib-resistant GIST. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Tumor cells favor aerobic glycolysis, a phenomenon observed when sufficient oxygen is available. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | This pathway generates less energy than mitochondrial oxidative phosphorylation, which occurs in healthy cells. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Tumor cells facilitate nucleic acid synthesis and promote rapid growth using the pentose phosphate pathway . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Several studies have reported on the association between this distinct metabolic fingerprint and various hallmarks, including tumor cells’ progression and resistance to chemotherapy [, , ]. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | In the context of GIST, there is a growing body of evidence suggesting that this cancer-specific metabolic paradigm influences tumor malignancy, tumor risk stratification, and resistance to imatinib [, , ]. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | However, the relationship between glycolysis and GIST remains unclear. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Here, we provide a brief overview and analysis of the role of glycolysis in GIST, laying special emphasis on potential avenues for metabolic research and underscoring its merit as an intriguing therapeutic target. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | GLUT serves as the initial rate-limiting step in cellular glucose metabolism. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Within the GLUT family, GLUT-1 predominantly regulates basal glucose uptake, ensuring the maintenance of foundational cellular glucose metabolism. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Thus, this transporter is essential in the modulation of cellular energy production . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | In the context of GIST, it has been demonstrated that elevated GLUT-1 expression corresponds to an increased tumor risk grade . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | In a study assessing CD63 (a significant protein of the transmembrane 4 superfamily and an exosomal marker) expression in conjunction with GLUT-1 expression, a significant correlation was found between GLUT-1 expression and CD63 expression in tumor cells among 54 patients with CD117(c-kit)-positive gastric GIST who had not undergone prior treatment with imatinib or other chemotherapy agents, and high levels of GLUT-1 and CD63 were associated with a substantial decrease in disease-free survival . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Conversely, another study examining the characteristics of small extracellular vesicles derived from GIST cells in the plasma of patients with GIST suggested a correlation between an unfavorable prognosis and elevated carcinoembryonic antigen levels and/or diminished GLUT-1 levels . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Notably, direct comparisons between the expression levels of GLUT-1 and the levels of GLUT-1 in small extracellular vesicles may not be feasible, possibly accounting for the discrepancy observed in the abovementioned two studies . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Here, we conducted a comparative analysis between GIST cell lines with secondary mutations in PDGFRA exon 12 and the GIST-T1 cell line. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Interestingly, our findings revealed that imatinib treatment led to the downregulation of GLUT-1 and other components of the glycolysis pathway in parental GIST-T1 cells, even at low concentrations. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | In contrast, imatinib treatment increased the expression of these components in imatinib-resistant cells . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Therefore, we considered that the glycolysis pathway is essential for the acquisition of imatinib resistance by GIST cells and for cell survival. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | GLUT-2 is predominantly localized in pancreatic beta cells, hepatocytes, and renal tubular cells, whereas GLUT-3 is mainly expressed in nervous tissues . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | In a study that assessed the potential advantages of continuous versus intermittent imatinib administration in mice implanted with an imatinib-resistant GIST cell line harboring a secondary mutation in KIT exon 17, cytoplasmic GLUT-2 expression was significantly elevated in the treated group compared with the untreated group. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Moreover, the cytoplasmic and membrane-bound GLUT-3 levels were significantly higher in the intermittent treatment group than in the continuous treatment group . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | However, the significance of these findings and their underlying mechanisms are yet to be fully elucidated. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | GLUT-4 is a high-capacity glucose transporter primarily found in nondividing cells, such as those in adipose tissue, skeletal muscle, and the myocardium . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | In a study conducted on 57 patients with GIST receiving neoadjuvant chemotherapy with imatinib, all patients exhibited detectable GLUT-4 levels before imatinib therapy. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | However, among 22 patients whose tumor samples were obtained during surgery after neoadjuvant chemotherapy, 19 showed decreased GLUT-4 expression . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Based on these data, imatinib was considered to interact with glycolysis and GLUT-4 expression. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Overall, these findings suggest that a multitude of GLUT subtypes are involved in the pathogenesis of imatinib resistance in GIST. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The upregulation of GLUT expression can play a vital role in the acquisition of imatinib resistance by GIST and cell survival. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | In addition to GLUT, hexokinase (HK), phosphofructokinase 1 (PFK1), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), pyruvate kinase (PK), lactate dehydrogenase (LDH), and monocarboxylate transporters (MCT) are recognized to be associated with glycolysis . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | A previous study demonstrated increased activity of HK1 (one of the HK isoforms), PKM2 (one of the PK isoforms), and LDH in high-risk grade tumors, suggesting their potential in the preoperative prediction of malignancy . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Furthermore, research into the association between MCT and GIST has unveiled the pronounced expression of MCT1, MCT2, and MCT4 . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The coexpression of MCT1 and its chaperone, CD147, has been implicated in the aggressiveness of GIST and correlated with reduced patient survival . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | While numerous studies have reported on the association between glycolysis-related molecules and various types of cancer, there has been a paucity of research focusing solely on GIST [, , ]. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | A summary of glycolysis-related molecules in GIST is shown in Table 1.Table 1Role of glycolytic molecules in gastrointestinal stromal tumor. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Table 1MoleculesAssociations and functionsReferencesGLUT-1Elevated GLUT-1 expression corresponds to heightened tumor risk grade19GLUT-1 expression positively correlates with CD63 expression18High GLUT-1 and CD63 levels in GIST cells correlate with lower disease-free survival18High carcinoembryonic antigen or low GLUT-1 in plasma small extracellular vesicles indicates poor prognosis23Imatinib reduced GLUT-1 in GIST-T1 cells but increased glycolysis in imatinib-resistant cells20GLUT-2In imatinib-treated mice with resistant GIST, GLUT-2 expression was higher than in untreated mice25GLUT-3Intermittent imatinib treatment increased GLUT-3 levels compared to continuous treatment in mice25GLUT-4Neoadjuvant imatinib therapy reduced GLUT-4 expression27HK, PK, LDHHK1, PKM2, and LDH activity elevated in high-risk grade19MCTMCT1 and CD147 coexpression are associated with GIST aggressiveness and reduced patient survival29GIST: gastrointestinal stromal tumor; GLUT: glucose transporter; HK: hexokinase; LDH: lactate dehydrogenase; MCT: monocarboxylate transporters; PK: pyruvate kinase Role of glycolytic molecules in gastrointestinal stromal tumor. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | GIST: gastrointestinal stromal tumor; GLUT: glucose transporter; HK: hexokinase; LDH: lactate dehydrogenase; MCT: monocarboxylate transporters; PK: pyruvate kinase F-Fluorodeoxyglucose positron emission tomography/computed tomography (F-FDG PET/CT) is one of the most commonly used functional imaging modalities in clinical practice. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | This technique uses a radioisotope to trace glucose and is recommended for GIST imaging . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The imaging diagnosis using F-FDG PET/CT is based on glucose metabolism in vivo . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The accumulation of the tracer is primarily mediated by GLUT . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Notably, FDG PET/CT has been demonstrated to have a high predictive prognostic value for recurrence-free survival in patients with localized primary GIST through assessment of preoperative metabolic tumor volume (MTV) and total lesion glycolysis (TLG) . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Regarding GIST patients with KIT exon 11 mutations, FDG PET/CT demonstrated that imatinib treatment reduces FDG uptake levels within 1–7 days post treatment . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Immunohistochemical findings have suggested the involvement of GLUT-4 in FDG uptake in GIST, which is confirmed by the decrease in GLUT-4 levels following imatinib therapy . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Additionally, in vitro treatment of GIST cells with imatinib caused translocation of GLUT-4 from the plasma membrane to the cytosol via endocytosis as shown by lower plasma membrane-bound GLUT-4 levels . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Imatinib directly affects glycolysis and GLUT-4 expression, thereby resulting in decreased FDG uptake . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | FDG uptake evaluations on preoperative PET/CT of 40 patients with GIST revealed positive correlations between FDG uptake and tumor size; tumor risk grade per the Fletcher classification; and GLUT-1, HK1, and LDHA expression levels . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Analyses were conducted on several metabolic parameters, including maximum standardized uptake value corrected for body weight (SUVbw), lean body mass (SUVlbm), and body surface area (SUVbsa), as well as MTV and TLG in 35 patients with GIST . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The study, which included 35 patients with GIST, aimed to assess the predictive capability of preoperative FDG PET/CT in determining the malignancy risk of GIST and the likelihood of recurrence and mortality. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Although there were no statistically significant associations between PET/CT metabolic parameters (SUVbw, SUVlbm, SUVbsa, MTV, and TLG) and patient demographics, tumor size, mitotic index, Ki-67, and tumor location, these parameters were positively correlated with the tumor risk grade per the Fletcher classification. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Moreover, MTV and TLG were identified as independent outcome predictors for progression-free survival . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The report of the aforementioned study suggests the profound involvement of molecules associated with glycolysis, including GLUT, in the risk of GIST malignancy and recurrence. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | However, the clinical utility of PET/CT in GIST remains unclear, and there is lack of direct evidence to show the extent of the effect of imatinib treatment on FDG uptake via downregulation of GLUT contributing to the risk of malignancy and recurrence of GIST. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | A summary of FDG PET/CT in GIST is shown in Table 2.Table 2Overview of F-Fluorodeoxyglucose positron emission tomography/computed. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Table 2:Associations and functionsReferencesFDG PET/CT, using preoperative MTV and TLG assessments, strongly predicts RFS in localized primary GIST patients36Imatinib treatment lowers FDG uptake within 1–7 days27Imatinib downregulates glycolysis and GLUT-4 expression, leading to reduced FDG uptake27, 37FDG uptake positive correlates with tumor size, Fletcher risk grade, and the expression of GLUT-1, HK1, and LDHA19PET/CT metabolic parameters (SUVbw, SUVlbm, SUVbsa, MTV, and TLG) positive correlate with Fletcher risk grade but not with patient background, tumor size, mitotic index, Ki-67, or location38MTV and TLG independently predict PFS outcomes38FDG: F-Fluorodeoxyglucose; GIST: gastrointestinal stromal tumor; GLUT: glucose transporter; HK: hexokinase; LDHA: lactate dehydrogenase; MTV: metabolic tumor volume; PET/CT: positron emission tomography/computed tomography; PFS: progression-free survival; RFS: recurrence-free survival; SUVbsa: standardized uptake value corrected for body surface area; SUVbw: standardized uptake value corrected for body weight; SUVlbm: standardized uptake value corrected for lean body mass; TLG: total lesion glycolysis Overview of F-Fluorodeoxyglucose positron emission tomography/computed. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | FDG: F-Fluorodeoxyglucose; GIST: gastrointestinal stromal tumor; GLUT: glucose transporter; HK: hexokinase; LDHA: lactate dehydrogenase; MTV: metabolic tumor volume; PET/CT: positron emission tomography/computed tomography; PFS: progression-free survival; RFS: recurrence-free survival; SUVbsa: standardized uptake value corrected for body surface area; SUVbw: standardized uptake value corrected for body weight; SUVlbm: standardized uptake value corrected for lean body mass; TLG: total lesion glycolysis Using GIST cell lines, validation studies revealed differences in the metabolic activity of glycolysis and oxidative phosphorylation (OXPHOS) between imatinib-sensitive GIST and imatinib-resistant GIST. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | However, these varied depending on the specific cell line examined. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | For instance, imatinib-resistant GIST 882 cells showed a distinct metabolic profile with increased levels of glycolysis and OXPHOS compared with their original parent cells. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | In contrast, imatinib-resistant cells derived from the GIST-T1 cell line had glycolytic activity that was comparable to that of their parent cells; however, their mitochondrial respiration was decreased. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Moreover, imatinib-resistant GIST 882 cells were more vulnerable to glycolysis inhibition than GIST 882 cells, whereas imatinib-resistant GIST-T1 cells were more resistant to OXPHOS inhibition than GIST-T1 cells . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The intertumor heterogeneity in the metabolic phenotype of imatinib-resistant GIST needs to further investigated. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Imatinib can influence the metabolic phenotype of GIST, potentially contributing to imatinib resistance. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | We also speculate that the observed differences in metabolic activity levels could be attributed to a process known as the reverse Warburg effect. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | In this mechanism, metabolites such as lactate and pyruvate are produced by oxidative stressed cancer-associated fibroblasts and are used by cancer cells for ATP synthesis within the mitochondria . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | However, no studies have confirmed the presence of this phenomenon in GIST. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Recent studies have highlighted the potential prognostic significance of various DNAs (KIT, PDGFRA, BRAF, SDH, SETD2, and ROR2) and microRNAs (miR-221, miR-222, miR-494, miR-196a, miR-320a, miR-218, miR-125a-5p, and miR-518a-5p) in GIST . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | However, only a few molecular markers have been developed for GIST prognosis. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | At present, there are no established circulating biomarkers associated with glycolysis . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Fig. 1 illustrates the relationship among GIST, glycolysis, and oxidative phosphorylation. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Fig. 1A schematic illustration of the relationship between gastrointestinal stromal tumor (GIST) and glycolysis and oxidative phosphorylation (OXPHS). |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Particularly, we focused on the relationship bwtween GIST and imatinib, a representative drug for treating GIST. |
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