title: Targeting MET in cancer: rationale and progress.
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.
authors.affiliation: Medical Research Council (MRC) Centre, Hills Road, Cambridge CB2 2QH, UK. egherard@mrc-lmb.cam.ac.uk
authors.forename: Ermanno
authors.initials: E
authors.lastname: Gherardi
authors.forename: Walter
authors.initials: W
authors.lastname: Birchmeier
authors.forename: Carmen
authors.initials: C
authors.lastname: Birchmeier
authors.forename: George
authors.initials: G
authors.lastname: Vande Woude
mesh_terms: D058750:Epithelial-Mesenchymal Transition; D017228:Hepatocyte Growth Factor / Q000378:metabolism / Q000502:physiology; D006801:Humans; D009369:Neoplasms / Q000235:genetics* / Q000473:pathology; D019859:Proto-Oncogene Proteins c-met / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D017228:Hepatocyte Growth Factor; D019859:Proto-Oncogene Proteins c-met