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dc.contributor.authorVenepalli, Neeta K.
dc.contributor.authorGoff, Laura
dc.date.accessioned2014-01-03T15:47:10Z
dc.date.available2014-01-03T15:47:10Z
dc.date.issued2013-03
dc.identifier.bibliographicCitationVenepalli NK, Goff L. Targeting the HGF-cMET Axis in Hepatocellular Carcinoma. International Journal of Hepatology. 2013;2013:341636. doi: 10.1155/2013/341636.en_US
dc.identifier.issn2090-3448
dc.identifier.urihttp://hdl.handle.net/10027/10975
dc.descriptionCopyright © 2013 N. K. Venepalli and L. 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. © 2013 by Hindawi Publishing Corporation, International Journal of Hepatology.en_US
dc.description.abstractUnder 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.en_US
dc.language.isoen_USen_US
dc.publisherHindawi Publishing Corporationen_US
dc.titleTargeting the HGF-cMET Axis in Hepatocellular Carcinomaen_US
dc.typeArticleen_US


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