^
    Contact us  to learn more about
    our Premium Content:  News alerts, weekly reports and conference planners
    BIOMARKER:

    MET elevation

    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
    7ms
    GENOME‐WIDE TRANSCRIPTOME ANALYSIS REVEALS KEY GENES AND PATHWAYS ASSOCIATED WITH THYROID CANCER METASTASIS (ATA 2023)
    BVE‐Met cells developed resistance to BRAFV600E inhibitor PLX4720, but remained sensitive to β‐catenin/KDM4A inhibitor PKF118‐310. In summary, we have identified several targetable genes/pathways in thyroid cancer metastasis. Given the complexity of metastatic cells in evasion of host immune response, simultaneously targeting more than one of these pathways (PDL1, Mertk, IL6, COX‐1/Tbxas1‐TXA2) may be warranted to achieve better therapeutic effect.
    PD(L)-1 Biomarker • IO biomarker
    |
    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • MET (MET proto-oncogene, receptor tyrosine kinase) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • AXL (AXL Receptor Tyrosine Kinase) • PD-1 (Programmed cell death 1) • IL6 (Interleukin 6) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • MERTK (MER Proto-Oncogene, Tyrosine Kinase) • CD44 (CD44 Molecule) • CD24 (CD24 Molecule) • CCL11 (C-C Motif Chemokine Ligand 11) • CCL2 (Chemokine (C-C motif) ligand 2) • CXCL5 (Chemokine (C-X-C motif) ligand 5) • IL5 (Interleukin 5)
    |
    PD-L1 expression • TP53 mutation • BRAF V600E • KRAS mutation • KRAS G12D • CDKN2A mutation • KRAS G12 • MERTK expression • CD44 expression • MET elevation • CD24 expression
    |
    PLX4720
    8ms
    The anti-oncogenic effect of 17-DMAG via the inactivation of HSP90 and MET pathway in osteosarcoma cells. (PubMed, Oncol Res)
    Based on the results of this study, we were able to confirm that 17-DMAG promotes inhibition of osteosarcoma cell proliferation and induction of apoptosis by inhibition of MET, a protein highly expressed in osteosarcoma cells. This approach may be useful for the establishment of a new treatment strategy for patients resistant to the standard treatment for osteosarcoma.
    Journal
    |
    MET (MET proto-oncogene, receptor tyrosine kinase) • HSP90AA1 (Heat Shock Protein 90 Alpha Family Class A Member 1Heat Shock Protein 90 Alpha Family Class A Member 1)
    |
    MET expression • MET elevation
    1year
    REGN5093 in Patients With MET-Altered Advanced Non-Small Cell Lung Cancer (clinicaltrials.gov)
    P1/2, N=82, Active, not recruiting, Regeneron Pharmaceuticals | Recruiting --> Active, not recruiting
    Enrollment closed • Metastases
    |
    MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    MET amplification • MET exon 14 mutation • MET mutation • MET expression • MET elevation
    |
    davutamig (REGN5093)
    over1year
    Expression of c-MET in Estrogen Receptor Positive and HER2 Negative Resected Breast Cancer Correlated with a Poor Prognosis. (PubMed, J Clin Med)
    In our series, high c-MET expression correlated with poor survival outcomes. Further studies are warranted to validate the clinical relevance and applicability of c-MET as a prognostic factor in ER+/HER2- early BC.
    Journal
    |
    HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • PGR (Progesterone receptor) • MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    HER-2 positive • ER positive • HER-2 negative • MET overexpression • MET expression • MET elevation • ER positive + HER-2 negative • PGR expression • MET-H
    almost2years
    Loss of Tpl2 activates compensatory signaling and resistance to EGFR/MET dual inhibition in v-RAS transduced keratinocytes. (PubMed, PLoS One)
    Inhibition of MET by Capmatinib increased p-EGFR in Tpl2-/- keratinocytes and papillomas, and inhibition of EGFR by Gefitinib increased HER2 and HER3 signaling in both genotypes. These data indicate that Tpl2 cross-talks with both EGFR and MET signaling pathways. Upon inhibition of EGFR/MET signaling, a myriad of escape mechanisms exists in keratinocytes to overcome targeted drug effects.
    Journal
    |
    EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • HRAS (Harvey rat sarcoma viral oncogene homolog) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • STAT3 (Signal Transducer And Activator Of Transcription 3) • MMP9 (Matrix metallopeptidase 9)
    |
    HRAS mutation • MET elevation
    |
    gefitinib • Tabrecta (capmatinib)