Clinical Development of c-MET Inhibition in Hepatocellular Carcinoma
Division of Medical Oncology, National Cancer Centre Singapore, 11 Hospital Drive, Singapore 169610, Singapore
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Author to whom correspondence should be addressed.
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These authors contributed equally to this work.
Academic Editor: Stephen L. Chan
Diseases 2015, 3(4), 306-324; https://doi.org/10.3390/diseases3040306
Received: 28 August 2015 / Revised: 4 October 2015 / Accepted: 21 October 2015 / Published: 28 October 2015
(This article belongs to the Special Issue Targeted Therapy of Hepatocellular Carcinoma: Present and Future)
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death. In patients with advanced or unresectable HCC, there are few treatment options. Conventional chemotherapy has limited benefits. Sorafenib, a multi-kinase inhibitor, improves survival, but options for patients intolerant of or progressing on sorafenib are limited. There has been much interest in recent years in molecular therapeutic targets and drug development for HCC. One of the more promising molecular targets in HCC is the cellular-mesenchymal-epithelial transition (c-MET) factor receptor. Encouraging phase II data on two c-MET inhibitors, tivantinib and cabozantinib, has led to phase III trials. This review describes the c-MET/hepatocyte growth factor (HGF) signalling pathway and its relevance to HCC, and discusses the preclinical and clinical trial data for inhibitors of this pathway in HCC.
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Keywords:
hepatocellular carcinoma (HCC); c-MET; hepatocyte growth factor (HGF); c-MET inhibitor; tivantinib; cabozantinib
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MDPI and ACS Style
Lee, J.J.X.; Chan, J.J.; Choo, S.P. Clinical Development of c-MET Inhibition in Hepatocellular Carcinoma. Diseases 2015, 3, 306-324.
AMA Style
Lee JJX, Chan JJ, Choo SP. Clinical Development of c-MET Inhibition in Hepatocellular Carcinoma. Diseases. 2015; 3(4):306-324.
Chicago/Turabian StyleLee, Joycelyn J.X.; Chan, Jack J.; Choo, Su P. 2015. "Clinical Development of c-MET Inhibition in Hepatocellular Carcinoma" Diseases 3, no. 4: 306-324.
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