Varaico: Literature-Extracted Genetic Variants

Gene:MET
Variant:p.Y1230C
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MET

NM_000245.4:p.Y1230C

Associated Papers

Targeting Mesenchymal-Epidermal Transition (MET) Aberrations in Non-Small Cell Lung Cancer: Current Challenges and Therapeutic Advances.

Deng F et al.

Cancers, 2026

Autoregulation of the MET receptor tyrosine kinase by its intracellular juxtamembrane domain.

Linossi EM et al.

The Biochemical Journal, 2025

MET Alterations in Cancer and MET-Targeted Therapy: Detection Strategies, Treatment Efficacy, and Emerging Technologies.

Park J et al.

Targeted Oncology, 2025

Evolving roles of MET as a therapeutic target in NSCLC and beyond.

Lee JB et al.

Nature Reviews. Clinical Oncology, 2025

A comprehensive database for identifying and interpreting ctDNA driver genes and variants in cancer.

Wang Y et al.

Scientific Data, 2025

40670358 (PubMed )
Supplement: 41597_2025_5550_MOESM1_ESM.xls › Table_S5

Challenges and resistance mechanisms to EGFR targeted therapies in head and neck cancers and breast cancer: Insights into RTK dependent and independent mechanisms.

Shyamsunder S et al.

Oncotarget, 2025

Antitumor Activity of Vebreltinib and Characterization of Clinicogenomic Features in Solid Tumors with MET Rearrangements.

Nakazawa S et al.

Cancer Discovery, 2025

Responsiveness of different MET tumour alterations to type I and type II MET inhibitors.

Murciano-Goroff YR et al.

Clinical and Translational Medicine, 2025

Targeting c-MET Alterations in Cancer: A Review of Genetic Drivers and Therapeutic Implications.

Ji M et al.

Cancers, 2025

Expert consensus on the diagnosis and treatment of non-small cell lung cancer with MET alteration.

Feng H et al.

Cancer Biology & Medicine, 2025

The expanding role of the receptor tyrosine kinase MET as a therapeutic target in non-small cell lung cancer.

Sattler M et al.

Cell Reports. Medicine, 2025

40020676 (PubMed )
Supplement: mmc2.pdf

Mapping kinase domain resistance mechanisms for the MET receptor tyrosine kinase via deep mutational scanning.

Estevam GO et al.

Elife, 2025

Characterization of Bozitinib as a potential therapeutic agent for MET-amplified gastric cancer.

Lin H et al.

Communications Biology, 2025

Plasma biomarkers for afatinib monotherapy in EGFR-mutated non-small cell lung cancer: Novel insights from companion genomics analysis of the EXTRA study.

Makiguchi T et al.

Cancer Treatment and Research Communications, 2025

A Concise Review of the Approved MET TKIs (Savolitinib, Gumarontinib, Vebreltinib, Tepotinib, Capmatinib) in China for MET Exon 14 Splice Site Mutated (METex14+) NSCLC Circa 2025.

Hu Y et al.

Lung Cancer (auckland, N.z.), 2025

Mapping kinase domain resistance mechanisms for the MET receptor tyrosine kinase via deep mutational scanning.

Estevam GO et al.

Biorxiv : the Preprint Server for Biology, 2024

Molecular profiling METex14+ non-small cell lung cancer (NSCLC): Impact of histology.

Marks JA et al.

Lung Cancer (amsterdam, Netherlands), 2024

Conserved regulatory motifs in the juxtamembrane domain and kinase N-lobe revealed through deep mutational scanning of the MET receptor tyrosine kinase domain.

Estevam GO et al.

Elife, 2024

Whole-Exome Sequencing Reveals Novel Candidate Driver Mutations and Potential Druggable Mutations in Patients with High-Risk Neuroblastoma.

Nokchan N et al.

Journal of Personalized Medicine, 2024

39338204 (PubMed )
Supplement: jpm-14-00950-s001.zip › Supplementary_Table_S5.xlsx › Supplementary_Table_S5.

Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors.

Pecci F et al.

Cancer Discovery, 2024

Conserved regulatory motifs in the juxtamembrane domain and kinase N-lobe revealed through deep mutational scanning of the MET receptor tyrosine kinase domain.

Estevam GO et al.

Biorxiv : the Preprint Server for Biology, 2024

Recording and classifying MET receptor mutations in cancers.

Guérin C et al.

Elife, 2024

The Efficacy and Safety of Treating Acquired MET Resistance Through Combinations of Parent and MET Tyrosine Kinase Inhibitors in Patients With Metastatic Oncogene-Driven NSCLC.

Patil T et al.

Jto Clinical and Research Reports, 2024

Targeting c-Met in breast cancer: From mechanisms of chemoresistance to novel therapeutic strategies.

Iweala EEJ et al.

Current Research in Pharmacology and Drug Discovery, 2024

Biophysical and structural characterization of the impacts of MET phosphorylation on tepotinib binding.

Grädler U et al.

The Journal of Biological Chemistry, 2023

MET in Non-Small-Cell Lung Cancer (NSCLC): Cross 'a Long and Winding Road' Looking for a Target.

Spitaleri G et al.

Cancers, 2023

The Development and Role of Capmatinib in the Treatment of MET-Dysregulated Non-Small Cell Lung Cancer-A Narrative Review.

Hsu R et al.

Cancers, 2023

The Preclinical Pharmacology of Tepotinib-A Highly Selective MET Inhibitor with Activity in Tumors Harboring MET Alterations.

Albers J et al.

Molecular Cancer Therapeutics, 2023

Molecular characterization of MET fusions from a large real-world Chinese population: A multicenter study.

Xia H et al.

Cancer Medicine, 2023

Overview of Molecular Detection Technologies for MET in Lung Cancer.

Heydt C et al.

Cancers, 2023

SYK-mediated epithelial cell state is associated with response to c-Met inhibitors in c-Met-overexpressing lung cancer.

Zhou J et al.

Signal Transduction and Targeted Therapy, 2023

Mutations in the MET tyrosine kinase domain and resistance to tyrosine kinase inhibitors in non-small-cell lung cancer.

Yao Y et al.

Respiratory Research, 2023

Preclinical Study of a Biparatopic METxMET Antibody-Drug Conjugate, REGN5093-M114, Overcomes MET-driven Acquired Resistance to EGFR TKIs in EGFR-mutant NSCLC.

Oh SY et al.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2023

Molecular pathways, resistance mechanisms and targeted interventions in non-small-cell lung cancer.

Wang Z et al.

Molecular Biomedicine, 2022

MET Signaling Pathways, Resistance Mechanisms, and Opportunities for Target Therapies.

Rivas S et al.

International Journal of Molecular Sciences, 2022

36430388 (PubMed )
Supplement: ijms-23-13898-s001.zip › ijms-1981646-supplementary.pdf

Refining patient selection of MET-activated non-small cell lung cancer through biomarker precision.

Lai GGY et al.

Cancer Treatment Reviews, 2022

Foretinib can overcome common on-target resistance mutations after capmatinib/tepotinib treatment in NSCLCs with MET exon 14 skipping mutation.

Fujino T et al.

Journal of Hematology & Oncology, 2022

The Occurrence of MET Ectodomain Shedding in Oral Cancer and Its Potential Impact on the Use of Targeted Therapies.

De Herdt MJ et al.

Cancers, 2022

Novel germline MET pathogenic variants in French patients with papillary renal cell carcinomas type I.

Sebai M et al.

Human Mutation, 2022

Utility of the Ba/F3 cell system for exploring on-target mechanisms of resistance to targeted therapies for lung cancer.

Koga T et al.

Cancer Science, 2022

Combination of Type I and Type II MET Tyrosine Kinase Inhibitors as Therapeutic Approach to Prevent Resistance.

Bahcall M et al.

Molecular Cancer Therapeutics, 2022

Non-small-cell lung cancer: how to manage MET exon 14 skipping mutant disease.

Blaquier JB et al.

Drugs in Context, 2022

Circulating tumour DNA biomarkers in savolitinib-treated patients with non-small cell lung cancer harbouring MET exon 14 skipping alterations: a post hoc analysis of a pivotal phase 2 study.

Yu Y et al.

Therapeutic Advances in Medical Oncology, 2022

Identification of a EML4-ALK exon 19 fusion variant in lung adenocarcinoma and alectinib resistance.

Liu D et al.

Lung Cancer (amsterdam, Netherlands), 2021

Brief Report: Heterogeneity of Acquired Resistance Mechanisms to Osimertinib and Savolitinib.

Lim SM et al.

Jto Clinical and Research Reports, 2021

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Regarding the variants extracted from papers and shown text snippets from research papers, the following holds: "Some rights reserved. This work permits non-commercial use, distribution and reproduction in any medium, provided the original author and source are credited."