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| Molecular Profile | KIT T417_D419delinsI |
| Therapy | Imatinib |
| Indication/Tumor Type | Advanced Solid Tumor |
| Response Type | conflicting |
| Molecular Profile | Indication/Tumor Type | Response Type | Therapy Name | Approval Status | Evidence Type | Efficacy Evidence | References |
|---|---|---|---|---|---|---|---|
| KIT T417_D419delinsI | Advanced Solid Tumor | conflicting | Imatinib | Preclinical - Cell culture | Actionable | In a preclinical study, Gleevec (imatinib mesylate) inhibited Kit phosphorylation in transformed cells over expressing KIT T417_D419delinsI in culture (PMID: 16015387). | 16015387 |
| KIT T417_D419delinsI | Advanced Solid Tumor | conflicting | Imatinib | Preclinical - Cell culture | Actionable | In a preclinical study, transformed cells expressing KIT T417_D419delinsI were resistant to treatment with Gleevec (imatinib) in culture (PMID: 24205792). | 24205792 |
| PubMed Id | Reference Title | Details |
|---|---|---|
| (24205792) | Flumatinib, a selective inhibitor of BCR-ABL/PDGFR/KIT, effectively overcomes drug resistance of certain KIT mutants. | Full reference... |
| (16015387) | Mutations in KIT and RAS are frequent events in pediatric core-binding factor acute myeloid leukemia. | Full reference... |