[Relationship between mutation on precore region of integrated HBV DNA and p53 gene mutation in hepatocellular carcinoma].
OBJECTIVE
The chronic infection of hepatitis B virus (HBV) is a recognized risk factor for the development of hepatocellular carcinoma (HCC); however, the precise mechanism of carcinogenesis is unknown. In order to better understand the molecular mechanism of hepatocarcinogenesis, this study was designed to investigate the relationship between the gene mutation on precore region of integrated HBV DNA, the mutation of p53 gene and the development of HCC.


METHODS
The integrated HBV DNA, gene mutation on precore region of HBV DNA and p53 gene mutation were detected in 80 specimens of HCC, paratumor cirrhosis, liver cirrhosis, and normal liver tissue using polymerase chain reaction (PCR) and single strand conformation polymorphism (SSCP) technique.


RESULTS
(1) The positive rates of integrated HBV DNA in HCC tissues, paratumor cirrhosis tissues, cirrhotic liver tissues, and normal liver tissues were 96.43%, 96.43%, 66.67%, and 6.66%, respectively. There were significant differences of the positive rates between normal liver tissues group and each of the other three groups (P< 0.005). (2) The gene mutation rates on precore region of HBV DNA in the four groups were 70.37%, 48.15%, 25.00%, and 0%, respectively. There were significant differences of the gene mutation rates among the four groups (P< 0.05). (3) The mutation rate (57.14%)of p53 gene in HCC was significantly higher than that in liver cirrhosis (16.67%) (P< 0.05). (4) The p53 gene mutation was positively associated with positivity of integrated HBV DNA and mutation on precore region of integrated HBV DNA in different liver tissues.


CONCLUSIONS
The HBV DNA integration and its gene mutation on precore region and p53 gene mutation probably play synergic roles in the development of HCC.
Wang
Xiu-Hai
XH
Department of Biology, The Qingdao University Medical College, Qingdao, Shandong, 266021, PR China. wangxiuhai@qingdaonews.com
Wang
Pei-Lin
PL
D000328:Adult; D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000209:etiology* / Q000235:genetics / Q000821:virology; D004279:DNA, Viral / Q000235:genetics*; D005260:Female; D016158:Genes, p53; D006515:Hepatitis B virus / Q000235:genetics*; D006801:Humans; D008113:Liver Neoplasms / Q000209:etiology* / Q000235:genetics / Q000821:virology; D008297:Male; D008875:Middle Aged; D009154:Mutation; D016133:Polymerase Chain Reaction; D018807:Polymorphism, Single-Stranded Conformational; D016662:Virus Integration
D004279:DNA, Viral