4.8 Article

Genetic variations of hepatitis B virus and serum aflatoxin-lysine adduct on high risk of hepatocellular carcinoma in Southern Guangxi, China

Journal

JOURNAL OF HEPATOLOGY
Volume 53, Issue 4, Pages 671-676

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.jhep.2010.04.032

Keywords

Hepatitis B virus; Genotype; BCP mutations; Aflatoxin-lysine adduct; Hepatocellular carcinoma

Funding

  1. National Cancer Institute [RO1 90997]

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Background & Aims: Southern Guangxi area is one of the endemic areas for hepatocellular carcinoma (HCC) in China. This study evaluates the roles of genetic variations of hepatitis B virus (HBV) and aflatoxin B-1 (AFB(1)) exposure in the formation of HCC in this high-risk area. Methods: The study recruited 60 HCC patients and 120 age-, gender-, and residency-nnatched controls. HBV genotype and basic core promoter (BCP) mutations were determined by nested-PCR/direct sequencing. Serum AFB(1)-lysine adduct was measured by high performance liquid chromatography-fluorescence detection. Results: HBV genotype C was predominant in 75.0% of cases and 84.2% of controls. The 1762(T)/1764(A) double mutations, 1753(V) mutations, and 1752(V) mutations were associated with HCC risk evidenced by the adjusted odds ratio (OR) [95% confidence interval (95% CI)] of 3.89 (1.40-10.77), 2.87 (1.49-5.49), and 5.96 (1.75-20.25), respectively. The adjusted OR (95% CI) was 6.94 (1.68-27.78) for subjects with 1762(T)/1764(A) double mutations and high AFB(1)-lysine adduct level; 2.01 (0.24-14.29), for those with only 1762(T)/1764(A) double mutations; and 4.26 (1.16-15.38) for those with only high AFB(1)-lysine adduct level, respectively. The adjusted OR was 5.13 (1.79-14.71) for subjects with 1753(V) mutations and high AFB(1)-lysine adduct level; 1.20 (0.47-3.08) for those with only 1753(V) mutations, and 2.28 (1.01-5.31) for those with high AFB(1)-lysine adduct level, respectively. Conclusions: These data confirmed the association of BCP mutations with HCC risk and the additive effects of 1762(T)/1764(A) double mutations and 1753(V) mutations with dietary AFB(1) exposure in this high-risk area for HCC. (C) 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

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