Missing content? – Request curation!
Request curation for specific Genes, variants, or PubMed publications.
Have questions, comments or suggestions? - Let us know!
Email us at : firstname.lastname@example.org
|Molecular Profile||Indication/Tumor Type||Response Type||Relevant Treatment Approaches||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|EML4 - ALK ALK L1196M ALK G1269A||Advanced Solid Tumor||resistant||Lorlatinib||Preclinical - Cell culture||Actionable||In a preclinical study, ALK L1196M was identified as a compound mutation in transformed cells expressing ALK G1269A in the context of EML4-ALK that acquired resistance to Lorlatinib (PF-06463922) in culture (PMID: 29650534).||29650534|
|EML4 - ALK ALK L1196M ALK G1269A||lung non-small cell carcinoma||predicted - resistant||Crizotinib||Case Reports/Case Series||Actionable||In a clinical study, a patient with non-small cell lung cancer harboring EML4-ALK demonstrated a partial response when treated with Xalkori (crizotinib), however, after 6 months the patient progressed and was found to harbor two secondary resistance mutations, ALK G1269A and ALK L1196M (PMID: 23344087).||23344087|
|Clinical Trial||Phase||Therapies||Title||Recruitment Status||Covered Countries||Other Countries|