Table of Contents
Hepatitis Research and Treatment
Volume 2011 (2011), Article ID 475965, 6 pages
http://dx.doi.org/10.1155/2011/475965
Research Article

TP53 Mutations and HBX Status Analysis in Hepatocellular Carcinomas from Iran: Evidence for Lack of Association between HBV Genotype D and TP53 R249S Mutations

1Mechanisms of Carcinogenesis Section, Molecular Carcinogenesis Group, International Agency for Research on Cancer, 150 Cours Albert Thomas, 69372 Lyon, France
2Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Kargar Shomali Avenue, 14117 Tehran, Iran

Received 4 May 2011; Accepted 18 June 2011

Academic Editor: Isabelle Chemin

Copyright © 2011 Behnoush Abedi-Ardekani et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

High incidence of HCC is mostly due to the combination of two major risk factors, chronic infection with hepatitis B (HBV) and/or C (HCV) viruses and exposure to the mycotoxin aflatoxin B1, which induces a particular mutation at codon 249 in TP53 (R249S). Eight genotypes of HBV are diversely found in high and low incidence areas. Regardless of documented strong associations between TP53 R249S mutation and HBV genotypes B, C, A or E, there is no report of such association for genotype D despite of the presence of aflatoxin in areas with high prevalence of HBV genotype D. In Iran, 3% of the population is chronically infected with HBV, predominantly genotype D. Twenty-one histologically confirmed HCC cases from Iran were analyzed for TP53 R249S and HBV double mutations 1762T/1764A, hallmarks of more pathogenic forms of HBV. We did not detect any of these mutations. In addition, we report the only case identified so far carrying both R249S mutation and chronic HBV genotype D, a patient from The Gambia in West Africa. This paper suggests that association between HBV genotype D and aflatoxin-induced TP53 mutation is uncommon, explaining the relatively lower incidence of HCC in areas where genotype D is highly prevalent.