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Molecular Profile | EML4 - ALK ALK G1202R |
Therapy | Lorlatinib |
Indication/Tumor Type | lung cancer |
Response Type | conflicting |
Molecular Profile | Indication/Tumor Type | Response Type | Therapy Name | Approval Status | Evidence Type | Efficacy Evidence | References |
---|---|---|---|---|---|---|---|
EML4 - ALK ALK G1202R | lung cancer | conflicting | Lorlatinib | Preclinical - Cell culture | Actionable | In a preclinical study, transformed cells expressing EML4-ALK with ALK G1202R were resistant to growth inhibition mediated by Lorlatinib (PF-06463922) in culture (PMID: 26698910). | 26698910 |
EML4 - ALK ALK G1202R | lung cancer | conflicting | Lorlatinib | Preclinical - Cell line xenograft | Actionable | In a preclinical study, Lorbrena (lorlatinib) inhibited Alk phosphorylation, reduced proliferation, and induced apoptosis in transformed cells over expressing ALK G1202R in the context of EML4-ALK in culture and in cell line xenograft models (PMID: 26144315). | 26144315 |
PubMed Id | Reference Title | Details |
---|---|---|
(26144315) | PF-06463922, an ALK/ROS1 Inhibitor, Overcomes Resistance to First and Second Generation ALK Inhibitors in Preclinical Models. | Full reference... |
(26698910) | Resensitization to Crizotinib by the Lorlatinib ALK Resistance Mutation L1198F. | Full reference... |