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|Molecular Profile||Indication/Tumor Type||Response Type||Relevant Treatment Approaches||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|FLT3 V592G||Advanced Solid Tumor||sensitive||FLT3 Inhibitor||Midostaurin||Preclinical - Cell culture||Actionable||In a preclinical study, Rydapt (midostaurin) inhibited FLT3-induced phosphorylation of ERK1/2 and reduced growth of transformed cells expressing FLT3 V592G in culture (PMID: 18068628).||18068628|
|FLT3 V592G||acute myeloid leukemia||predicted - sensitive||FLT3 Inhibitor||Sorafenib||Case Reports/Case Series||Actionable||In a clinical case study, Nexavar (sorafenib) and Droxia (hydroxyurea) treatment resulted in complete remission with no minimal residual disease, and continued Nexavar (sorafenib) treatment plus Vidaza (azacytidine) treatment resulted in sustained response for at least 60 months in a patient with acute myeloid leukemia harboring FLT3 V592G, along with NPM1 W288fs and TET2 T556fs (PMID: 32984009).||32984009|