Research Papers:
Molecular alterations in hepatocellular carcinoma associated with hepatitis B and hepatitis C infections
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Abstract
Maria Lina Tornesello1,*, Luigi Buonaguro1,*, Francesco Izzo2, Franco M. Buonaguro1
1Molecular Biology and Viral Oncology Unit, Department of Research, Istituto Nazionale Tumori “Fondazione G. Pascale” - IRCCS, Napoli, Italy
2Hepato-Biliary Surgery Department, Istituto Nazionale Tumori “Fondazione G. Pascale” - IRCCS, Napoli, Italy
*These authors have contributed equally to this work
Correspondence to:
Maria Lina Tornesello, e-mail: [email protected]
Keywords: hepatitis C virus (HCV), hepatitis B virus (HBV), hepatocellular carcinoma (HCC), genetic alteration, somatic mutation
Received: September 15, 2015 Accepted: February 20, 2016 Published: March 02, 2016
ABSTRACT
Chronic infections with hepatitis B (HBV) and hepatitis C viruses (HCV) are the leading cause of cirrhosis and hepatocellular carcinoma (HCC) worldwide. Both viruses encode multifunctional regulatory proteins activating several oncogenic pathways, which induce accumulation of multiple genetic alterations in the infected hepatocytes. Gene mutations in HBV- and HCV-induced HCCs frequently impair the TP53, Wnt/b-catenin, RAS/RAF/MAPK kinase and AKT/mTOR pathways, which represent important anti-cancer targets. In this review, we highlight the molecular mechanisms underlying the pathogenesis of primary liver cancer, with particular emphasis on the host genetic variations identified by high-throughput technologies. In addition, we discuss the importance of genetic alterations, such as mutations in the telomerase reverse transcriptase (TERT) promoter, for the diagnosis, prognosis, and tumor stratification for development of more effective treatment approaches.
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