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International Journal of HepatologyVolume 2013 2013, Article ID 341636, 11 pages

Review Article

Division of Hematology-Oncology, University of Illinois at Chicago, 840 South Wood Street, Suite 820-E, MC 713, Chicago, IL 60612, USA

Hematology-Oncology Fellowship Program, Division of Hematology-Oncology, Vanderbilt Ingram Cancer Center, 777 Preston Research Building, Nashville, TN 37232-6307, USA

Received 28 November 2012; Accepted 11 March 2013

Academic Editor: Pierluigi Toniutto

Copyright © 2013 Neeta K. Venepalli and Laura Goff. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Under normal physiological conditions, the hepatocyte growth factor HGF and its receptor, the MET transmembrane tyrosine kinase cMET, are involved in embryogenesis, morphogenesis, and wound healing. The HGF-cMET axis promotes cell survival, proliferation, migration, and invasion via modulation of epithelial-mesenchymal interactions. Hepatocellular cancer HCC is the third most common cause of worldwide cancer-related mortality; advanced disease is associated with a paucity of therapeutic options and a five-year survival rate of only 10%. Dysregulation of the HGF-cMET pathway is implicated in HCC carcinogenesis and progression through activation of multiple signaling pathways; therefore, cMET inhibition is a promising therapeutic strategy for HCC treatment. The authors review HGF-cMET structure and function in normal tissue and in HCC, cMET inhibition in HCC, and future strategies for biomarker identification.

Autor: Neeta K. Venepalli and Laura Goff



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