Published online Nov 28, 2014. doi: 10.3748/wjg.v20.i44.16464
Revised: June 24, 2014
Accepted: August 13, 2014
Published online: November 28, 2014
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.