Jiang CM, Pu CW, Hou YH, Chen Z, Alanazy M, Hebbard L. Non alcoholic steatohepatitis a precursor for hepatocellular carcinoma development. World J Gastroenterol 2014; 20(44): 16464-16473 [PMID: 25469014 DOI: 10.3748/wjg.v20.i44.16464]
Corresponding Author of This Article
Dr. Lionel Hebbard, Senior Research Fellow, Liver Cancer and Metabolism Group Head, Storr Liver Unit, Westmead Millennium Institute, University of Sydney, PO Box 412, Darcy Road, Westmead, NSW 2145, Australia. lionel.hebbard@sydney.edu.au
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Topic Highlight
Open-Access Policy of This Article
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Chun-Meng Jiang, Ya-Hui Hou, Department of Digestive System, the Second Affiliated Hospital of Dalian Medical University, Dalian 116023, Liaoning Province, China
Chun-Wen Pu, Department of Liver Disease, Dalian the Sixth People’s Hospital, Dalian 116033, Liaoning Province, China
Zhe Chen, Department of General Surgery, the Second Affiliated Hospital of Dalian Medical University, Dalian 116023, Liaoning Province, China
Mohammed Alanazy, Lionel Hebbard, Storr Liver Unit, Westmead Millennium Institute, University of Sydney, Westmead NSW 2145, Australia
Author contributions: Jiang CM and Pu CW contributed equally to this work; and all authors reviewed the final version of this paper.
Supported by Robert W Storr Bequest to the Sydney Medical Foundation University of Sydney (LH), Cancer Council NSW grant 1069733 (LH) and the West Translational Cancer Research Centre Partner Program funded by the Cancer Institute, NSW
Correspondence to: Dr. Lionel Hebbard, Senior Research Fellow, Liver Cancer and Metabolism Group Head, Storr Liver Unit, Westmead Millennium Institute, University of Sydney, PO Box 412, Darcy Road, Westmead, NSW 2145, Australia. lionel.hebbard@sydney.edu.au
Telephone: +61-2-98459132 Fax: +61-2-98459103
Received: May 5, 2014 Revised: June 24, 2014 Accepted: August 13, 2014 Published online: November 28, 2014
Abstract
Hepatocellular carcinoma (HCC) is increasing in prevalence and is one of the most common cancers in the world. Chief amongst the risks of attaining HCC are hepatitis B and C infection, aflatoxin B1 ingestion, alcoholism and obesity. The later has been shown to promote non alcoholic fatty liver disease, which can lead to the inflammatory form non alcoholic steatohepatitis (NASH). NASH is a complex metabolic disorder that can impact greatly on hepatic function. The mechanisms by which NASH promotes HCC are only beginning to be characterized. Here in this review, we give an overview of the recent novel mechanisms published that have been associated with NASH and subsequent HCC progression. We will focus our discussion on inflammation and gut derived inflammation and how they contribute to NASH driven HCC.
Core tip: Non alcoholic steatohepatitis (NASH) is a metabolic inflammatory disease the can often advance to liver cancer. Previously, it was assumed that obesity, hepatocyte cellular death and insulin resistance were the dominant drivers of NASH progression to hepatocellular carcinoma. Herein, we discuss the latest concepts concerning the gut microbiome and bile acids, which have now been shown to have a role in promoting hepatic inflammation, and subsequent liver tumor growth.
