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    BIOMARKER:

    ALK E1129V

    i
    Other names: NBLST3, CD246, Anaplastic Lymphoma Kinase, Anaplastic Lymphoma Kinase (Ki-1), CD246 Antigen, Mutant Anaplastic Lymphoma Kinase, ALK, ALK Receptor Tyrosine Kinase, Anaplastic Lymphoma Receptor Tyrosine Kinase, ALK Tyrosine Kinase Receptor
    Entrez ID:
    238
    Related biomarkers:
    Expression
    Mutation
    CNA
    Fusion
    Others
    over2years
    MET and NF2 alterations confer early resistance to first-line alectinib treatment in ALK-rearranged non-small cell lung cancer (ESMO 2022)
    Of these, 52 received first-line alectinib treatment (1L) and 56 received alectinib after crizotinib resistance (2L). Also, NF2-mutant patients only had a median PFS of 4 months, significantly poorer than those without (HR 11.1, 95CI 2.17-50; p<0.001). Conclusions By analyzing different mutational profiles of ALK-rearranged patients after alectinib treatment, we proposed MET and NF2 as putative mechanisms that conferred resistance to early resistance of first-line alectinib, which shone light on future tailored treatment for ALK-positive NSCLCs.
    Clinical
    |
    KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • NRAS (Neuroblastoma RAS viral oncogene homolog) • NF2 (Neurofibromin 2)
    |
    KRAS mutation • BRAF mutation • NRAS mutation • PIK3CA mutation • ALK positive • MET amplification • ALK rearrangement • ALK mutation • MET mutation • ALK G1202R • NF2 mutation • ALK G1269A • ALK I1171N • ALK I1171T • ALK I1171 • ALK L1196M • ALK amplification • ALK V1180L • ALK E1129V • ALK rearrangement + PIK3CA mutation • MET D1228H
    |
    Xalkori (crizotinib) • Alecensa (alectinib)