Published online Feb 14, 2016. doi: 10.3748/wjg.v22.i6.1943
Peer-review started: April 13, 2015
First decision: June 26, 2015
Revised: July 27, 2015
Accepted: November 9, 2015
Article in press: December 1, 2015
Published online: February 14, 2016
Core tip: The tumorigenesis of hepatitis B virus-associated hepatocellular carcinoma (HCC) has been widely studied. The preS/S mutants are considered “precursor lesions” of HCC. Different preS/S mutants induce various mechanisms of tumorigenesis, such as transactivation and an inflammatory response. The preS2 mutants and type II “Ground Glass” hepatocytes represent novel biomarkers of HCC. The preS mutants may induce the unfolded protein response and endoplasmic reticulum stress-dependent and stress-independent pathways. Treatments to inhibit hepatitis B surface antigen (HBsAg) and damage secondary to HBsAg or the preS/S mutants include antivirals and antioxidants. Methods for the prevention and treatment of HCC should be comprehensive.