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Trends Cell Biol. 2009 Oct;19(10):542-51. doi: 10.1016/j.tcb.2009.07.002. Epub 2009 Sep 14.

Crosstalk in Met receptor oncogenesis.

Author information

1
Department of Biochemistry, McGill University, Montreal, Quebec, Canada.

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.

PMID:
19758803
DOI:
10.1016/j.tcb.2009.07.002
[Indexed for MEDLINE]

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