The association between mutations in the reverse transcriptase domain of hepatitis B virus polymerase gene with tumorigenesis of hepatocellular carcinoma
10.3781/j.issn.1000-7431.2014.02.007
- Author:
Fu-Min GAO
1
Author Information
1. Department of Epidemiology
- Publication Type:Journal Article
- Keywords:
DNA mutational analysis;
Epidemiologic methods;
Hepatitis B virus;
Liver neoplasms
- From:
Tumor
2014;34(2):141-146
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore the relationship between the mutations in the reverse transcriptase (RT) domain of hepatitis B virus polymerase (HBV-P) gene and the occurrence and development of hepatocellular carcinoma (HCC). Methods: In this case-control study, the serum samples from 202 HCC patients and 202 chronic hepatitis B virus (CHB) carriers matching for age and gender were collected. The sequence of the RT domain of HBV-P gene was determined by direct sequencing following PCR amplification. The relationship between the mutations in the RT domain of HBV-P gene and the occurrence and development of HCC was analyzed. Results: The T895A, A904T and C955T mutations in the RT domain of HBV-P gene were all significantly associated with HCC compared to non-HCC controls (P = 0.034, 47.5% vs 37.1%; P = 0.011, 5.4% vs 1.0%; P = 0.030, 5.4% vs 1.5%). Furthermore, the Logistic multivariate analysis showed that T895A was an independent risk factor for HCC [odds ratio (OR) = 2.230, 95% confidence interval (CI): 1.230-4.044, P = 0.008]. A904T or C955T increased the risk of HCC occurrence either (OR = 6.523, 95% CI: 0.838-50.733; OR = 2.904, 95% CI: 0.599-14.093), but it did not reach statistical significance. The mutation rate of combined mutation occurrence either in A904 or C955T was 9.4% in HCC group and 2.5% in non-HCC controls (P = 0.003). The adjusted OR was 4.145 (95% CI: 1.170-14.681), demonstrating its significant association with HCC (P = 0.028). Conclusion: The mutations in the RT domain of HBV-P gene are associated with the tumorigenesis of HCC. Copyright © 2014 by TUMOR.
