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- W2062110561 abstract "The hepatocyte growth factor (HGF) and its receptor, the transmembrane tyrosine kinase cMET, promote cell proliferation, survival, motility, and invasion as well as morphogenic changes that stimulate tissue repair and regeneration in normal cells but can be co-opted during tumor growth. MET overexpression, with or without gene amplification, has been reported in a variety of human cancers, including breast, lung, and GI malignancies. Furthermore, high levels of HGF and/or cMET correlate with poor prognosis in several tumor types, including breast, ovarian, cervical, gastric, head and neck, and non–small-cell lung cancers. Gene amplification and protein overexpression of cMET drive resistance to epidermal growth factor receptor family inhibitors, both in preclinical models and in patients. It is increasingly apparent that the HGF-cMET axis signaling network is complex, and rational combinatorial therapy is needed for optimal clinical efficacy. Better understanding of HGF-cMET axis signaling and the mechanism of action of HGF-cMET inhibitors, along with the identification of biomarkers of response and resistance, will lead to more effective targeting of this pathway for cancer therapy." @default.
- W2062110561 created "2016-06-24" @default.
- W2062110561 creator A5005221518 @default.
- W2062110561 creator A5073488441 @default.
- W2062110561 creator A5077579849 @default.
- W2062110561 date "2012-09-10" @default.
- W2062110561 modified "2023-10-18" @default.
- W2062110561 title "Targeting the Hepatocyte Growth Factor–cMET Axis in Cancer Therapy" @default.
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- W2062110561 doi "https://doi.org/10.1200/jco.2011.40.3774" @default.
- W2062110561 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3434988" @default.
- W2062110561 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22869872" @default.
- W2062110561 hasPublicationYear "2012" @default.