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- W2016146051 abstract "The Met receptor tyrosine kinase (RTK) regulates several distinct biological processes, including cell scatter, cell invasion, cell survival and epithelial remodeling. MET is genetically altered through several mechanisms in multiple human cancers; these events are causally related to cancer initiation and progression, identifying Met as a potential therapeutic target. Recent evidence highlights additional roles for Met in cancer through crosstalk with other receptors and cell surface proteins. In this review, we discuss recent progress in our understanding of mechanisms of interaction between Met, the epidermal growth factor receptor family and other cell surface protein families, and how these contribute to signal crosstalk, oncogenesis and drug resistance. The Met receptor tyrosine kinase (RTK) regulates several distinct biological processes, including cell scatter, cell invasion, cell survival and epithelial remodeling. MET is genetically altered through several mechanisms in multiple human cancers; these events are causally related to cancer initiation and progression, identifying Met as a potential therapeutic target. Recent evidence highlights additional roles for Met in cancer through crosstalk with other receptors and cell surface proteins. In this review, we discuss recent progress in our understanding of mechanisms of interaction between Met, the epidermal growth factor receptor family and other cell surface protein families, and how these contribute to signal crosstalk, oncogenesis and drug resistance." @default.
- W2016146051 created "2016-06-24" @default.
- W2016146051 creator A5016753271 @default.
- W2016146051 creator A5029137680 @default.
- W2016146051 creator A5088293962 @default.
- W2016146051 date "2009-10-01" @default.
- W2016146051 modified "2023-09-30" @default.
- W2016146051 title "Crosstalk in Met receptor oncogenesis" @default.
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