PMCID string | Title string | Sentences string |
|---|---|---|
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | LMTK3 also accelerates the translation rate of the KIT gene, resulting in secondary mutations that further leads to KIT resistance to IM . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | The auto-phosphorylation of KIT mutant is spatiotemporally regulated. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | The fully transformed products of KIT mutants, KIT onco-proteins were usually in the endoplasmic reticulum, transferring to the Golgi apparatus and activated as an immature KIT protein form [149–151]. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Protein kinase C (PKC) is a superfamily characteristic of phospholipid-dependent serine-threonine kinases. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | It physiologically regulates cell stability and differentiation. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | As one member of PKC, Protein kinase C-θ (PKC-θ) is highly expressed in the ICCs of the digestive tracts of guinea pigs, and in GIST ranging from 72 to 98% . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | PKC-θ promotes the Golgi complex retention of mutant-KITs and blocks its proteasomal degradation, thus sustains the activation of abnormally localized intracellular activation of MT-KITs . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | PKC-θ over-expression was significantly positively correlated with KIT expression and poor clinicopathological characteristics and worse prognosis . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Mutations on KIT often result in abnormal activation of kinases that activate downstream MAPK, STATs and PI3K pathways, promoting tumorigenesis and malignant progression . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | The genes correlated with the Hedgehog (Hh) pathway are robustly expressed in ICC stem cells and mature cells of human and murine intestines, indicating its indispensable role in the development of epithelium and mesenchymal cells in GI tract. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Physiologically, the ligands (HHs), sonic Hedgehog (Shh), Indian Hedgehog (Ihh), and Desert Hedgehog (Dhh), bind to the receptors, Patched-1 (Ptch-1) and Patched-2 (Ptch-2), respectively, thereby initiating the Hh pathway . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Loss of the 7-pass transmembrane protein Smoothened (SMO) inhibition leads to the regulation of Hh pathway which controls the expression levels of KIT mRNA via its downstream glioma-associated oncogene homolog isoform1, 2, and 3(GLI1, 2, or 3) . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | In the absence of ligand, SMO starts to activate the hedgehog pathway . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Various GLI1, 2, and 3 have different roles in the expression of KIT mRNA. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | GLI1/2 up-regulate the KIT mRNA level, while GLI3 is a transcriptional repressor on KIT mRNA levels via the proteasome pathway . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Besides, the Hh pathway has crosstalk with PI3K/AKT/mTOR and RAF/MAPK/ERK signal cascades involved in the KIT regulation . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | In vivo, targeting the Hh pathway can reduce KIT mRNA and re-enhance the sensitivity of GIST cells to TKIs. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | PI3K pathway is the dominant signal directly engaged by mutant KIT oncogenic cascade in GIST, therefore, PI3K inhibitors showed meaningful efficacy when combined with IM is ongoing in the clinical trials for the treatment of GIST . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | In mutant KITs, they direct active themselves and engaging PI3K pathway to promote imatinib resistance. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | For example, in double-mutant KitV558Δ; Y567F/Y567F knock-in mice which lack the SRC family kinase-binding site on KIT (pY567) exhibited attenuated MAPK signaling, and engagement of the PI3K pathway for tumor growth , as shown in Table 1. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Phosphoinositide-3-kinase, regulatory subunit 3 (gamma) (PIK3R3, p55PIK) is a regulatory subunit of phosphoinositide 3-kinase (PI3K) and is involved in ICC hyperplasia which is prone to the tumorigenesis of GIST . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Over-expression of p55PIK in GIST882 cells bind the promoter and increase the expression of NF-κB p65 (Ser536), leading to resultant KIT upregulation. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Similar mechanism of p55PIK activating the NF-κB signal was also observed in the colorectal cancer cells . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Non-RTK activated CDC42 associated kinase 1 (ACK1), was colocalized and form complex with KIT protein in GIST cells and ACK1 activation is in a partially KIT and CDC42 dependent manner. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Treatment with a specific ACK1 inhibitor AIM-100 or ACK1 siRNA markedly inhibits cell migration in imatinib sensitive and in imatinib resistant GIST cell lines, which is associated with inactivation of PI3K/AKT/mTOR and RAF/MAPK signaling pathways . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Recently, a study of PD-1/PD-L1 blockade rescue exhausted CD8 + T cells via the PI3K/Akt/mTOR signaling pathway in GIST revealing the involvement of PI3K in immunotherapy in GIST . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Fibroblast growth factors (FGFs) and their receptors (FGFR1-4) are universally expressed in human tissues and have an important effect on various cell physiologic processes ranging from cell proliferation, survival, and migration. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | The dysregulation of the FGFs signal pathway is extensively involved in several types of cancers . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | FGF2 is highly expressed in Imatinib-resistant GIST cells and the tumor tissue from the patients who progressed on Imatinib . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | FGF2 binds to and activates its receptors FGFR, mediating the reactivation of KIT and MAPK pathways . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | The opening of CTCF binding in the chromosome topology of FGF and KIT mentioned above leads to the increase of their expression, which may demonstrate the close relationship between FGF and KIT in the development of resistance in GIST. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | The Janus kinase/signal transducers and activators of transcription (JAK/ STAT) pathway is one of the important downstream pathways by KIT activating . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | KIT D816V and KIT N882 both are situated closely on the KIT receptor activation loop activating the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, but in KIT N822K it is also the downstream activation of the MAPK . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | The V558Δ; V653A mutant mislocalization of Golgi, and lead to the enhanced activation of STAT3 and STAT5, although no differences were seen in MAPK or PI3K pathway activation, therefore, contributing to the increased tumor oncogenesis, compared to control mice with a single V558Δ Kit mutation. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Blocking KIT’s localization to the Golgi from the endoplasmic reticulum (ER) can inhibit oncogenic signaling . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | AMPD3, belonging to the adenosine monophosphate deaminases (AMPDs), functions as a main catalyzer which hydrolytically deaminates AMP to inosine monophosphate. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | This is a vital step in nucleotide metabolism aiding and energy balance in cells. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | AMPD3 is extensively expressed in tumor tissues, and its knockdown may favor the activation of AMPK, and subsequently result in the inhibition of the anabolic pathways which is prerequisite for the survival of cancer cell . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | AMPD3 is significantly related to KIT expression in GIST. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Interestingly, when the expression of KIT or AMPD3 was suppressed by siRNA, respectively, the expression of AMPD3 or KIT was also comparably decreased. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | These results indicate that KIT and AMPD3 may form a positive protein–protein feedback loop to promote their reciprocal expression, albeit their underlying mechanism remaining unknown . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Limb Expression 1 (LIX1) is a unique marker of digestive mesenchyme immaturity. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | It regulates mesenchymal progenitor proliferation and differentiation by controlling the Hippo effector Yes-associated protein 1 (YAP1), which is constitutively activated in many sarcomas . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | In GIST, upon LIX1 inactivation in GIST cells, YAP1/TAZ activity is reduced, KIT, as the GIST signature, is down-regulated via reducing YAP1/TAZ protein level, and cells acquire smooth muscle lineage features . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Moreover, LIX1 can controls MAPK signaling pathway . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Upon the condition of hypoxia during IM treatment in GIST, hypoxia inducible factor 1 alpha (HIF-1α) can increase the transcription level of MET gene via its bind to the MET promoter . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Ligation of upregulated MET by hepatocyte growth factor (HGF) expand the activation of the downstream of mitogen-activated protein kinase (MAPK). |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | And the latter then stabilizes ETV1 for promoting KIT expression . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | These results strongly suggested that reactivation of MAPK by bypass signal may represent a therapeutic vulnerability for targeting KIT expression. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | In screening a compound library enriched for U.S FDA-approved chemotherapeutic agents, GIST cells displayed high sensitivity to transcriptional inhibitors, and mechanistically, these compounds exploited the cells dependency on continuous KIT expression. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | For example, Mithramycin A inhibits the TF, SP1, which is also a major transcriptional activation of the KIT gene, thus explaining why Mithramycin A induces apoptosis . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | These indicated that it is plausible to target KIT abnormal regulatory-circus, together with kinase activity-inhibition in GIST treatment (Fig. 3).Fig. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | 3The mechanism of action of existing drugs targeting KIT expression and mutations. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | In this figure we describe several inhibitors targeting KIT expression and function. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Therapeutic strategies of TKIs targeting KIT mutations in gastrointestinal stromal tumors: fist-line therapy-Imatinib; second-line therapy-Sunitinib; third-line therapy-Regorafenib; fourth-line therapy-Ripretinib. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Other new drugs targeting KIT mutations in gastrointestinal stromal tumors: Avapritinib, Larotrectinib, Entrectinib, Bezuclastinib, Carbozantinib, Sorafenib. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | The c-KIT-Hsp90Β-Apaf-1 complex inhibits the ubiquitination degradation of mutant KIT. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Bortezomib binds to Cbl, destabilizing the c-KIT-Hsp90Β-Apaf-1 complex and releasing Apaf-1, and then KIT proteins are internalized and degraded in GIST cells. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | IPI-504, IPI-493, TAS-116, AT13387 and NVP-AUY922 are HSP90 inhibitors. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | HDAC inhibitors, SAHA and LBH589, attenuate the activity of HSP90 by acetylating on HSP90 gene. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | For Hh pathway, HHs, SMO and GI1/2 have their own inhibitors. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | PI3K/mTOR inhibitor voxtalisib, the pan-PI3K inhibitor pilaralisib, and the PI3K-restricted inhibitor alpelisib all reducing GIST cell proliferation. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | TAT-N24 and the emerging PI3K or P55PIK inhibitors, such as Copanlisib, both inhibit NF -κB. BGJ398, PD173074 and nintedanib are FGFR inhibitor targeting FGFR1-4. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | ACK1 inhibitor AIM-100 or ACK1 siRNA inhibits ACK1. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | CS-1 and CS-2 are functioned as FTO inhibitors preventing KIT m6A mRNA demethylation. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | BBIs can reverse the transcription abnormalities of KIT gene which are induced by BRD4. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Mithramycin A inhibits the TF, SP1, and HZ1 decreases the transcriptions of OSR1 The mechanism of action of existing drugs targeting KIT expression and mutations. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | In this figure we describe several inhibitors targeting KIT expression and function. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Therapeutic strategies of TKIs targeting KIT mutations in gastrointestinal stromal tumors: fist-line therapy-Imatinib; second-line therapy-Sunitinib; third-line therapy-Regorafenib; fourth-line therapy-Ripretinib. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Other new drugs targeting KIT mutations in gastrointestinal stromal tumors: Avapritinib, Larotrectinib, Entrectinib, Bezuclastinib, Carbozantinib, Sorafenib. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | The c-KIT-Hsp90Β-Apaf-1 complex inhibits the ubiquitination degradation of mutant KIT. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Bortezomib binds to Cbl, destabilizing the c-KIT-Hsp90Β-Apaf-1 complex and releasing Apaf-1, and then KIT proteins are internalized and degraded in GIST cells. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | IPI-504, IPI-493, TAS-116, AT13387 and NVP-AUY922 are HSP90 inhibitors. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | HDAC inhibitors, SAHA and LBH589, attenuate the activity of HSP90 by acetylating on HSP90 gene. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | For Hh pathway, HHs, SMO and GI1/2 have their own inhibitors. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | PI3K/mTOR inhibitor voxtalisib, the pan-PI3K inhibitor pilaralisib, and the PI3K-restricted inhibitor alpelisib all reducing GIST cell proliferation. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | TAT-N24 and the emerging PI3K or P55PIK inhibitors, such as Copanlisib, both inhibit NF -κB. BGJ398, PD173074 and nintedanib are FGFR inhibitor targeting FGFR1-4. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | ACK1 inhibitor AIM-100 or ACK1 siRNA inhibits ACK1. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | CS-1 and CS-2 are functioned as FTO inhibitors preventing KIT m6A mRNA demethylation. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | BBIs can reverse the transcription abnormalities of KIT gene which are induced by BRD4. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Mithramycin A inhibits the TF, SP1, and HZ1 decreases the transcriptions of OSR1 Clinically, both HAND and BARX1 can be positive predictors for the progression or relapse events in the patients with metastatic GIST or post-operation GIST, respectively. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | HAND was enriched in small intestine ICCs while BARX1 was enriched in micro-GIST , thereby offering site-dependent targets for GIST treatment. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | In vivo, ETV1 is a critical survival factor for the growth of Imatinib-sensitive and Imatinib-resistant GIST cell lines . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Double inhibition of MAP kinase and KIT signaling can synergistically destabilize ETV1 by interrupting the positive feedback loop of KIT-MEK-ETV1-KIT. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Recent Phase II clinical trial showed an overall response of 69.0% and median progression free survival of 29.9 ms in the treatment-naïve patients with advanced GIST using MEK inhibitor Binimetinib plus Imatinib . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | In addition, SHBP2 and FOXF1 could be an ideal target for being further explored therapeutically in the treatment of GIST. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Phenothiazine is a cytotoxic drug that induces apoptosis and autophagy that showed synergistic role with ERK-inhibitor in the treatment of GIST . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | CDK7 mRNA and protein levels are elevated in high-risk GIST and indicated of poor clinical outcomes, in which CDK7 is a key activator of RNAPII that preferentially dysregulate RNAPII CTD phosphorylation. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | THZ1 blocks the role of CDK7 on RNAPII, and thus decrease the transcriptions of odd-skipped related transcription factor 1(OSR1), which is one of super enhancer (SE) of KIT gene in GIST . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Similarly, KIT-regulated enhancer domain in GIST could be targeted by BRD4, a crucial activator of RNAPII transcription at active chromatin marks, and the BBIs can reverse the transcription abnormalities of targeted genes which are induced by BRD4 . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | The combination of BBI and TKI led to superior cytotoxic effects in vitro and in vivo, with the advantage of preventing tumor growth in TKI-resistant GIST xenografts. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | The expression profiles of GIST cells treated with BBIs were akin to those treated with KIT inhibition, indicating the KIT expression be the target of BBIs . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Also, BET bromodomain is becoming an attractive target for KIT-mutant GIST as shown in clinical trials. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | A synthetic analogue of cerulenin, JQ1, has been shown to potently inhibit BRD4 and exhibited synergy with imatinib and induced apoptosis and autophagy in vitro . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Epi-transcriptional modifications on mRNA mainly influence its stability and expression, several molecules function as “writers” or “erasers” for the regulation of mRNA. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | Our previous study showed that FTO inhibition can dramatically inhibit cell proliferation and increase sensitivity of GIST cells to IM-induced apoptosis. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | CS-1 and CS-2 were recently repurposed as a FTO inhibitor and exhibited the synergistic effect with IM in KIT-mutated GIST . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | With the successful development of mRNA COVID-19 vaccines and the approval of a number of novel RNA-based drugs, RNA has jumped to the forefront of drug research . |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | In addition to mRNA's role in producing antigens or therapeutic proteins, different types of RNA have a variety of functions and play important regulatory roles in cells and tissues. |
PMC10898159 | KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST | One type of these RNAs, lncRNAs, has the potential to be used as new therapies, and the lncRNA itself can be used as both drugs and targets. |
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