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|Ref Type||Journal Article|
|Authors||Sa JK, Hong JY, Lee IK, Kim JS, Sim MH, Kim HJ, An JY, Sohn TS, Lee JH, Bae JM, Kim S, Kim KM, Kim ST, Park SH, Park JO, Lim HY, Kang WK, Her NG, Lee Y, Cho HJ, Shin YJ, Kim M, Koo H, Kim M, Seo YJ, Kim JY, Choi MG, Nam DH, Lee J|
|Title||Comprehensive pharmacogenomic characterization of gastric cancer.|
|Abstract Text||Gastric cancer is among the most lethal human malignancies. Previous studies have identified molecular aberrations that constitute dynamic biological networks and genomic complexities of gastric tumors. However, the clinical translation of molecular-guided targeted therapy is hampered by challenges. Notably, solid tumors often harbor multiple genetic alterations, complicating the development of effective treatments.To address such challenges, we established a comprehensive dataset of molecularly annotated patient derivatives coupled with pharmacological profiles for 60 targeted agents to explore dynamic pharmacogenomic interactions in gastric cancers.We identified lineage-specific drug sensitivities based on histopathological and molecular subclassification, including substantial sensitivities toward VEGFR and EGFR inhibition therapies in diffuse- and signet ring-type gastric tumors, respectively. We identified potential therapeutic opportunities for WNT pathway inhibitors in ALK-mutant tumors, a significant association between PIK3CA-E542K mutation and AZD5363 response, and transcriptome expression of RNF11 as a potential predictor of response to gefitinib.Collectively, our results demonstrate the feasibility of drug screening combined with tumor molecular characterization to facilitate personalized therapeutic regimens for gastric tumors.|
|Molecular Profile||Treatment Approach|
|Gene Name||Source||Synonyms||Protein Domains||Gene Description||Gene Role|
|Therapy Name||Drugs||Efficacy Evidence||Clinical Trials|
|Drug Name||Trade Name||Synonyms||Drug Classes||Drug Description|
|Gene||Variant||Impact||Protein Effect||Variant Description||Associated with drug Resistance|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|PIK3CA E542K||stomach cancer||sensitive||Capivasertib||Case Reports/Case Series||Actionable||In a clinical case study, treatment with Truqap (capivasertib) in a patient with gastric cancer harboring PIK3CA E542K resulted in a partial response, and in preclinical studies, led to decreased cell proliferation in a gastric cancer cell line harboring PIK3CA E542K (PMID: 32070411).||32070411|
|PIK3CA E545K||stomach cancer||sensitive||Capivasertib||Preclinical - Cell culture||Actionable||In a preclinical study, a gastric cancer cell line harboring PIK3CA E545K was sensitive to treatment with Truqap (capivasertib), demonstrating decreased cell proliferation in culture (PMID: 32070411).||32070411|