title: Met decoys: will cancer take the bait?
abstract: Inappropriate Met receptor tyrosine kinase signaling can produce proliferative, invasive, angiogenic, and antiapoptotic activities that contribute to malignant growth. Met can be activated by paracrine or autocrine mechanisms in a ligand-dependent fashion, or be constitutively activated by mutation and by other ligand-independent mechanisms. Because Met is inappropriately expressed in almost all types of human cancer, the HGF/SF-Met signaling pathway should be an exceptional target for cancer intervention strategies and therapies. In this issue of Cancer Cell, two reports show that the extracellular domain of Met is an important target for developing anticancer therapies.
authors.affiliation: Laboratory of Molecular Oncology, Van Andel Research Institute, 333 Bostwick NE, Grand Rapids, Michigan 49503, USA.
authors.forename: Yu-Wen
authors.initials: YW
authors.lastname: Zhang
authors.forename: Carrie
authors.initials: C
authors.lastname: Graveel
authors.forename: Nariyoshi
authors.initials: N
authors.lastname: Shinomiya
authors.forename: George F
authors.initials: GF
authors.lastname: Vande Woude
mesh_terms: D000818:Animals; D006801:Humans; D009369:Neoplasms / Q000378:metabolism* / Q000628:therapy; D019859:Proto-Oncogene Proteins c-met / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D019859:Proto-Oncogene Proteins c-met