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Targeting MET in cancer: rationale and progress

Official URL:https://doi.org/10.1038/nrc3205
PubMed:View item in PubMed
Creators Name:Gherardi, E. and Birchmeier, W. and Birchmeier, C. and Woude, G.V.
Journal Title:Nature Reviews Cancer
Journal Abbreviation:Nat Rev Cancer
Page Range:89-103
Date:February 2012
Keywords:Epithelial-Mesenchymal Transition, Hepatocyte Growth Factor, Neoplasms, Proto-Oncogene Proteins c-met, Signal Transduction
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.
Publisher:Nature Publishing Group (U.K.)
Additional Information:Erratum in: Nat Rev Cancer 12(9): 637.
Item Type:Review

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