Associated Papers
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
38564707 (PubMed )
Supplement: cd-23-1217_supplementary_table_3_suppst3.pdf
Identification of pathogenic missense mutations using protein stability predictors.
Gerasimavicius L et al.
Scientific Reports, 2020
32958805 (PubMed )
Supplement: 41598_2020_72404_MOESM2_ESM.xlsx › ClinVar
MET-dependent solid tumours - molecular diagnosis and targeted therapy.
Guo R et al.
Nature Reviews. Clinical Oncology, 2020
Therapeutic Efficacy of ABN401, a Highly Potent and Selective MET Inhibitor, Based on Diagnostic Biomarker Test in MET-Addicted Cancer.
Kim J et al.
Cancers, 2020
Glesatinib Exhibits Antitumor Activity in Lung Cancer Models and Patients Harboring MET Exon 14 Mutations and Overcomes Mutation-mediated Resistance to Type I MET Inhibitors in Nonclinical Models.
Engstrom LD et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2017
The role of the c-Met pathway in lung cancer and the potential for targeted therapy.
Sattler M et al.
Therapeutic Advances in Medical Oncology, 2011
Genome-wide analysis to predict protein sequence variations that change phosphorylation sites or their corresponding kinases.
Ryu GM et al.
Nucleic Acids Research, 2009
19139070 (PubMed )
Supplement: gkn1008_nar-01723-s-2008-File009.xls › TypeI-
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