Topic Highlight
Copyright ©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Mar 21, 2008; 14(11): 1741-1748
Published online Mar 21, 2008. doi: 10.3748/wjg.14.1741
DNA methylation in hepatocellular carcinoma
Iris Tischoff, Andrea Tannapfel
Iris Tischoff, Andrea Tannapfel, Institute of Pathology, Ruhr-University of Bochum, Bürkle-de-la-Camp-Platz 1, Bochum 44789, Germany
Correspondence to: Iris Tischoff, MD, Institute of Pathology, Ruhr-University of Bochum, Bürkle-de-la-Camp-Platz 1, Bochum 44789, Germany. iris.tischoff@rub.de
Telephone: +49-234-3024955
Fax: +49-234-3024809
Received: October 30, 2007
Revised: January 5, 2008
Published online: March 21, 2008
Abstract

As for many other tumors, development of hepatocellular carcinoma (HCC) must be understood as a multistep process with accumulation of genetic and epigenetic alterations in regulatory genes, leading to activation of oncogenes and inactivation or loss of tumor suppressor genes (TSG). In the last decades, in addition to genetic alterations, epigenetic inactivation of (tumor suppressor) genes by promoter hypermethylation has been recognized as an important and alternative mechanism in tumorigenesis. In HCC, aberrant methylation of promoter sequences occurs not only in advanced tumors, it has been also observed in premalignant conditions just as chronic viral hepatitis B or C and cirrhotic liver. This review discusses the epigenetic alterations in hepatocellular carcinoma focusing DNA methylation.

Keywords: Hepatocellular carcinoma; DNA methylation; Histone modification; Tumor suppressor genes