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Novel therapeutic inhibitors of the c-Met signaling pathway in cancer Eder JP; Vande Woude GF; Boerner SA; LoRusso PMClin Cancer Res 2009[Apr]; 15 (7): 2207-14A wide variety of human malignancies exhibit sustained c-Met stimulation, overexpression, or mutation, including carcinomas of the breast, liver, lung, ovary, kidney, and thyroid. Notably, activating mutations in c-Met have been positively identified in patients with a particular hereditary form of papillary renal cancer, directly implicating c-Met in human tumorigenesis. Aberrant signaling of the c-Met signaling pathway due to dysregulation of the c-Met receptor or overexpression of its ligand, hepatocyte growth factor (HGF), has been associated with an aggressive phenotype. Extensive evidence that c-Met signaling is involved in the progression and spread of several cancers and an enhanced understanding of its role in disease have generated considerable interest in c-Met and HGF as major targets in cancer drug development. This has led to the development of a variety of c-Met pathway antagonists with potential clinical applications. The three main approaches of pathway-selective anticancer drug development have included antagonism of ligand/receptor interaction, inhibition of the tyrosine kinase catalytic activity, and blockade of the receptor/effector interaction. Several c-Met antagonists are now under clinical investigation. Preliminary clinical results of several of these agents, including both monoclonal antibodies and small-molecule tyrosine kinase inhibitors, have been encouraging. Several multitargeted therapies have also been under investigation in the clinic and have demonstrated promise, particularly with regard to tyrosine kinase inhibition.|Antibodies, Monoclonal/therapeutic use[MESH]|Antineoplastic Agents/*therapeutic use[MESH]|Hepatocyte Growth Factor/antagonists & inhibitors[MESH]|Humans[MESH]|Neoplasms/drug therapy/enzymology[MESH]|Protein Kinase Inhibitors/*therapeutic use[MESH]|Proto-Oncogene Proteins c-met/*antagonists & inhibitors/metabolism[MESH]|Signal Transduction/drug effects[MESH] |
