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    BIOMARKER:

    ALK F1174L

    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
    Impact of compound mutations I1171N + F1174I and I1171N + L1198H on the structure of ALK in NSCLC pathogenesis: atomistic insights. (PubMed, J Biomol Struct Dyn)
    In contrast to wild conformation, the mutant conformations exhibited a reduced node degree in their residue interaction networks. Collectively, our findings provide deeper insights into the deleterious effects of I1171N + F1174I and I1171N + L1198H ALK compound mutations, which may contribute to NSCLC pathogenesis.Communicated by Ramaswamy H. Sarma.
    Journal
    |
    ALK (Anaplastic lymphoma kinase)
    |
    ALK positive • ALK fusion • ALK mutation • ALK F1174L • ALK I1171N • ALK I1171 • ALK F1174I
    almost3years
    Deciphering the Mechanism of Gilteritinib Overcoming Lorlatinib Resistance to the Double Mutant I1171N/F1174I in Anaplastic Lymphoma Kinase. (PubMed, Front Cell Dev Biol)
    These discrepancies created the capacity of the double mutant ALK I1171N/F1174I to confer drug resistance to lorlatinib. Our result anticipates to provide a mechanistic insight into the mechanism of drug resistance induced by ALK I1171N/F1174I that are resistant to lorlatinib treatment in NSCLC.
    Journal
    |
    ALK (Anaplastic lymphoma kinase)
    |
    ALK F1174L • ALK I1171N • ALK I1171 • ALK F1174I
    |
    Lorbrena (lorlatinib) • Xospata (gilteritinib)
    almost4years
    Gilteritinib overcomes lorlatinib resistance in ALK-rearranged cancer. (PubMed, Nat Commun)
    Surprisingly, EML4-ALK I1171N + F1174I compound mutant-expressing tumors were not completely shrunk but regrew within a short period of time after alectinib or lorlatinib treatment. However, the relapsed tumor was markedly shrunk after switching to the gilteritinib in vivo model. In addition, gilteritinib was effective against NTRK-rearranged cancers including entrectinib-resistant NTRK1 G667C-mutant and ROS1 fusion-positive cancer.
    Journal
    |
    ALK (Anaplastic lymphoma kinase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK1 (Neurotrophic tyrosine kinase, receptor, type 1) • EML4 (EMAP Like 4) • NTRK (Neurotrophic receptor tyrosine kinase)
    |
    NTRK1 fusion • ALK rearrangement • ALK mutation • ROS1 fusion • ROS1 positive • ALK F1174L • ALK I1171N • ALK I1171 • NTRK1 mutation • ALK F1174I • NTRK1 G667C
    |
    Rozlytrek (entrectinib) • Alecensa (alectinib) • Lorbrena (lorlatinib) • Xospata (gilteritinib)