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- A A Oyagbemi, O I Azeez, and A B Saba.
- Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, Oyo State, Nigeria. ademolaoyagbemi@yahoo.com
- Afr Health Sci. 2010 Mar 1; 10 (1): 939893-8.
AbstractThe incidence of hepatocellular carcinoma is increasing worldwide as well as the associated risk factors, some of which include exposure to aflatoxin B1, Hepatitis B (HBV) virus and hepatitis C (HCV) virus. Mutation of tumour suppressor gene p53 at codon 249(ser) at exon 7 has been found to contribute significantly to replication of damaged DNA and subsequent tumour progression. The x gene of HBV (HBx) is the most common open reading frame integrated into the host genome in hepatocellular carcinoma and the integrated HBx is frequently mutated in hepatocellular carcinoma. Mutant HBx proteins still retain their ability to bind to p53 thereby attenuating DNA repair and p53-mediated apoptosis.
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