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BIOMARKER:

MET N375S

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:
over3years
MET Mutation Is a Potential Therapeutic Target for Advanced Endometrial Cancer. (PubMed, Cancers (Basel))
MET N375S mutation is a germline variant that causes chemoresistance to cisplatin, with a high incidence in Eastern Asia. This study highlights the ethnic differences in the biology of the disease, which can influence treatment recommendations and the genome-guided clinical trials of advanced endometrial cancer.
Journal
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KRAS (KRAS proto-oncogene GTPase) • MET (MET proto-oncogene, receptor tyrosine kinase) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • HGF (Hepatocyte growth factor) • CHEK2 (Checkpoint kinase 2) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1)
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KRAS mutation • MET mutation • CBL mutation • CHEK2 mutation • U2AF1 mutation • MET N375S
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cisplatin
over3years
[VIRTUAL] Germline Polymorphisms Guide Cancer Therapy: Example of METN375S in Squamous Cell Carcinoma of the Head and Neck (CSI-FCS 2020)
Consequently, METN375S positive cells confer resistance to MET inhibitors like crizotinib, but are sensitive to HER2 blockade including afatinib and trastuzumab. This is being validated in a clinical trial of HER2 inhibition in patients with SCCHN and lung and who harbour the METN375S Polymorphism.
BRCA Biomarker • PARP Biomarker • IO biomarker
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EGFR (Epidermal growth factor receptor) • BRCA (Breast cancer early onset)
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EGFR mutation • MET N375S
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Herceptin (trastuzumab) • Xalkori (crizotinib) • Gilotrif (afatinib)
over4years
Clinical • New P2 trial
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TP53 (Tumor protein P53) • MET (MET proto-oncogene, receptor tyrosine kinase)
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TP53 mutation • HER-2 amplification • MET amplification • MET mutation • MET N375S
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Gilotrif (afatinib)
over4years
A common MET polymorphism harnesses HER2 signaling to drive aggressive squamous cell carcinoma. (PubMed, Nat Commun)
Accordingly, HER2 blockers, but not c-MET inhibitors, are paradoxically effective at restraining in vivo and in vitro models expressing MET. These results establish MET as a biologically distinct and clinically actionable molecular subset of SCCs that are uniquely amenable to HER2 blocking therapies.
Journal
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HER-2 (Human epidermal growth factor receptor 2)
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MET expression • MET N375S
over4years
Tissue gene mutation profiles in patients with colorectal cancer and their clinical implications. (PubMed, Biomed Rep)
TP53 mutations were more common in patients ≥60 years old (P<0.05), and IDH1 mutations were more common in male patients (P<0.05). NGS 50 gene panel sequencing provides a comprehensive tissue gene mutation profile which may significantly improve clinical management.
Clinical • Journal
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • STK11 (Serine/threonine kinase 11) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • SMAD4 (SMAD family member 4)
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TP53 mutation • KRAS mutation • PIK3CA mutation • STK11 mutation • KIT mutation • KRAS G12A • MET mutation • KRAS G12 • MET N375S