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| Molecular Profile | EML4 - ALK ALK C1156Y ALK L1198F |
| Therapy | Crizotinib |
| Indication/Tumor Type | Advanced Solid Tumor |
| Response Type | sensitive |
| Molecular Profile | Indication/Tumor Type | Response Type | Therapy Name | Approval Status | Evidence Type | Efficacy Evidence | References |
|---|---|---|---|---|---|---|---|
| EML4 - ALK ALK C1156Y ALK L1198F | Advanced Solid Tumor | sensitive | Crizotinib | Preclinical - Cell culture | Actionable | In a preclinical study, Xalkori (crizotinib) treatment inhibited viability of transformed cells expressing EML4-ALK with ALK C1156Y and ALK L1198F in culture (PMID: 35726063). | 35726063 |
| EML4 - ALK ALK C1156Y ALK L1198F | Advanced Solid Tumor | sensitive | Crizotinib | Preclinical - Cell culture | Actionable | In a preclinical study, Xalkori (crizotinib) inhibited growth of transformed cells expressing EML4-ALK with ALK C1156Y and ALK L1198F in culture (PMID: 26698910). | 26698910 |
| PubMed Id | Reference Title | Details |
|---|---|---|
| (26698910) | Resensitization to Crizotinib by the Lorlatinib ALK Resistance Mutation L1198F. | Full reference... |
| (35726063) | Analysis of lorlatinib analogs reveals a roadmap for targeting diverse compound resistance mutations in ALK-positive lung cancer. | Full reference... |