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    BIOMARKER:

    MET H1094Y

    i
    Other names: DFNB97, AUTS9, RCCP2, C-Met, HGFR, HGF Receptor, Met Proto-Oncogene, HGF/SF Receptor, Proto-Oncogene C-Met, Scatter Factor Receptor, Tyrosine-Protein Kinase Met, Hepatocyte Growth Factor Receptor, MET, MET Proto-Oncogene, Receptor Tyrosine Kinase
    Entrez ID:
    4233
    Related biomarkers:
    Expression
    Mutation
    CNA
    Fusion
    Others
    over1year
    Safety and efficacy of crizotinib in MET mutated (METmut) advanced non-small cell lung Cancer (aNSCLC): Results from the Drug Rediscovery Protocol (DRUP) (ESMO 2023)
    Conclusions Crizotinib proved highly effective in pts with METmut aNSCLC, with a manageable toxicity profile. Additional research is warranted to identify biomarkers for response.
    Clinical • Metastases
    |
    ALK (Anaplastic lymphoma kinase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS)
    |
    MET exon 14 mutation • MET mutation • MET H1094Y
    |
    Xalkori (crizotinib)
    almost2years
    Activating MET Kinase Domain Mutations Define a Novel Targetable Molecular Subtype of Non-small Cell Lung Cancer that is Clinically Sensitive to MET Inhibitor Elzovantinib (TPX-0022) (IASLC-TTLC 2023)
    "CONCLUSION Activating MET TKD mutations without concurrent MET exon 14 mutations were detected in ~ 0.2% of NSCLC, and occur in the absence of other known drivers in a subset of cases. Comprehensive genomic profiling to detect these alterations and guide treatment selection and clinical trial enrollment is warranted."
    Clinical
    |
    EGFR (Epidermal growth factor receptor) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase)
    |
    KRAS mutation • MET amplification • EGFR amplification • MET exon 14 mutation • MET H1094Y • MET D1228N • MET F1200I
    |
    elzovantinib (TPX-0022)
    almost2years
    Mutations in the MET tyrosine kinase domain and resistance to tyrosine kinase inhibitors in non-small-cell lung cancer. (PubMed, Respir Res)
    MET TKD mutations were identified in both baseline and patients treated with TKIs. MET-H1094Y might play an oncogenic role in NSCLC and may confer acquired resistance to EGFR-TKIs. Preliminary data indicates that EGFR-mutated NSCLC patients who acquired MET-V1092I or MET-H1094Y may benefit from combinatorial therapy with EGFR-TKI and MET-TKI, providing insights into personalized medical treatment.
    Journal
    |
    MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    EGFR mutation • MET amplification • MET exon 14 mutation • MET mutation • MET H1094Y • MET D1228N • MET D1228H • MET Y1230C