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Targeting MET in cancer: rationale and progress

Item Type:Review
Title:Targeting MET in cancer: rationale and progress
Creators Name:Gherardi, E. and Birchmeier, W. and Birchmeier, C. and Woude, G.V.
Abstract:Uncontrolled cell survival, growth, angiogenesis and metastasis are essential hallmarks of cancer. Genetic and biochemical data have demonstrated that the growth and motility factor hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, the tyrosine kinase MET, have a causal role in all of these processes, thus providing a strong rationale for targeting these molecules in cancer. Parallel progress in understanding the structure and function of HGF/SF, MET and associated signalling components has led to the successful development of blocking antibodies and a large number of small-molecule MET kinase inhibitors. In this Review, we discuss these advances, as well as results from recent clinical studies that demonstrate that inhibiting MET signalling in several types of solid human tumours has major therapeutic value.
Keywords:Epithelial-Mesenchymal Transition, Hepatocyte Growth Factor, Neoplasms, Proto-Oncogene Proteins c-met, Signal Transduction
Source:Nature Reviews Cancer
ISSN:1474-175X
Publisher:Nature Publishing Group (U.K.)
Volume:12
Number:2
Page Range:89-103
Date:February 2012
Additional Information:Erratum in: Nat Rev Cancer 12(9): 637.
Official Publication:https://doi.org/10.1038/nrc3205
PubMed:View item in PubMed

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