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World J Gastroenterol. Feb 28, 2016; 22(8): 2494-2502
Published online Feb 28, 2016. doi: 10.3748/wjg.v22.i8.2494
Hepatocellular carcinoma and non-alcoholic steatohepatitis: The state of play
Bérénice Charrez, Liang Qiao, Lionel Hebbard
Bérénice Charrez, Lionel Hebbard, Department of Molecular and Cell Biology, James Cook University, Townsville, QLD 4811, Australia
Liang Qiao, Lionel Hebbard, Westmead Millennium Institute, Westmead Hospital and University of Sydney, Sydney, NSW 2006, Australia
Author contributions: All authors contributed to this work.
Supported by The Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney; National Health and Medical Research Council of Australia (NHMRC) Project Grants (No. 1047417, to Qiao L; No. 1087297, to Hebbard L); and Cancer Council NSW Project Grants (No. 1070076, to Qiao L; No. 1069733, to Hebbard L).
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Lionel Hebbard, Senior Lecturer, Department of Molecular and Cell Biology, James Cook University, Townsville, QLD 4811, Australia. lionel.hebbard@jcu.edu.au
Telephone: +61-7-47815684
Received: November 2, 2015
Peer-review started: November 4, 2015
First decision: November 27, 2015
Revised: December 18, 2015
Accepted: December 30, 2015
Article in press: December 30, 2015
Published online: February 28, 2016
Processing time: 115 Days and 0.1 Hours
Abstract

Hepatocellular carcinoma (HCC) is now the fifth cancer of greatest frequency and the second leading cause of cancer related deaths worldwide. Chief amongst the risks of HCC are hepatitis B and C infection, aflatoxin B1 ingestion, alcoholism and obesity. The latter can promote non-alcoholic fatty liver disease (NAFLD), that can lead to the inflammatory form non-alcoholic steatohepatitis (NASH), and can in turn promote HCC. The mechanisms by which NASH promotes HCC are only beginning to be characterized. Here in this review, we give a summary of the recent findings that describe and associate NAFLD and NASH with the subsequent HCC progression. We will focus our discussion on clinical and genomic associations that describe new risks for NAFLD and NASH promoted HCC. In addition, we will consider novel murine models that clarify some of the mechanisms that drive NASH HCC formation.

Keywords: Non-alcoholic steatohepatitis; Hepatocellular carcinoma; Non-alcoholic fatty liver disease; Models; Mice

Core tip: Non-alcoholic steatohepatitis (NASH) is a metabolic inflammatory disease that can advance to liver cancer. Clinical studies have suggested links between non-alcoholic fatty liver disease, NASH and progression to hepatocellular carcinoma (HCC). Herein, we discuss genomic screens that have illustrated new candidate genes as markers for increased HCC risk. In addition, we present the latest murine models concerning cellular stress and inflammation, which have now been shown to have a role in promoting liver tumor growth.