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Molecular Profile | EML4 - ALK ALK G1269A |
Therapy | Alectinib |
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 |
---|---|---|---|---|---|---|---|
EML4 - ALK ALK G1269A | Advanced Solid Tumor | conflicting | Alectinib | Preclinical - Cell culture | Actionable | In a preclinical study, Alecensa (alectinib) inhibited viability of transformed cells expressing EML4-ALK with ALK G1269A in culture (PMID: 33627640). | 33627640 |
EML4 - ALK ALK G1269A | Advanced Solid Tumor | conflicting | Alectinib | Preclinical - Cell culture | Actionable | In a preclinical study, transformed cells expressing EML4-ALK with ALK G1269A were resistant to Alecensa (alectinib) mediated growth inhibition in culture (PMID: 27009859). | 27009859 |
EML4 - ALK ALK G1269A | Advanced Solid Tumor | conflicting | Alectinib | Preclinical - Cell culture | Actionable | In a preclinical study, transformed cells expressing EML4-ALK with ALK G1269A demonstrated resistance to Alecensa (alectinib) in culture (PMID: 25727400). | 25727400 |
EML4 - ALK ALK G1269A | Advanced Solid Tumor | conflicting | Alectinib | Preclinical - Cell line xenograft | Actionable | In a preclinical study, Alecensa (alectinib) inhibited growth of transformed cells expressing EML4-ALK with ALK G1269A in culture, and inhibited tumor growth in xenograft models (PMID: 24887559). | 24887559 |
EML4 - ALK ALK G1269A | Advanced Solid Tumor | conflicting | Alectinib | Preclinical - Cell culture | Actionable | In a preclinical study, Alecensa (alectinib) modestly inhibited growth of transformed cells expressing EML4-ALK with ALK G1269A in culture (PMID: 26698910). | 26698910 |
PubMed Id | Reference Title | Details |
---|---|---|
(25727400) | Activity of second-generation ALK inhibitors against crizotinib-resistant mutants in an NPM-ALK model compared to EML4-ALK. | Full reference... |
(27009859) | TKI sensitivity patterns of novel kinase-domain mutations suggest therapeutic opportunities for patients with resistant ALK+ tumors. | Full reference... |
(26698910) | Resensitization to Crizotinib by the Lorlatinib ALK Resistance Mutation L1198F. | Full reference... |
(24887559) | Selective ALK inhibitor alectinib with potent antitumor activity in models of crizotinib resistance. | Full reference... |
(33627640) | Gilteritinib overcomes lorlatinib resistance in ALK-rearranged cancer. | Full reference... |