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

Genetic variations of hepatitis B virus and serum aflatoxin-lysine adduct on high risk of hepatocellular carcinoma in Southern Guangxi, China.
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DOI:
10.1016/j.jhep.2010.04.032
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发表时间:
2010-10
影响因子:
25.7
通讯作者:
Wang JS
Wang JS
中科院分区:
医学1区
文献类型:
--
作者:
Xu L;Qian G;Tang L;Su J;Wang JS

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桂南地区是我国肝癌的高发区之一。本研究评估了乙型肝炎病毒 (HBV) 和黄曲霉毒素 B1 (AFB1) 暴露的遗传变异在该高风险地区 HCC 形成中的作用。该研究招募了 60 名 HCC 患者和 120 名年龄、性别、居住地相匹配的对照者。通过巢式 PCR/直接测序确定 HBV 基因型和基本核心启动子 (BCP) 突变。采用高效液相色谱-荧光检测法测定血清AFB1-赖氨酸加合物。 HBV 基因型 C 在 75.0% 的病例和 84.2% 的对照中占主导地位。 1762T/1764A 双突变、1753V 突变和 1752V 突变与 HCC 风险相关,调整后的比值比 (OR) [95% 置信区间 (95% CI)] 为 3.89 (1.40–10.77)、2.87 (1.49–5.49) 和 5.96 (1.75–20.25),分别。对于具有 1762T/1764A 双突变且 AFB1-赖氨酸加合物水平较高的受试者,调整后的 OR (95% CI) 为 6.94 (1.68–27.78); 2.01 (0.24–14.29),对于仅具有 1762T/1764A 双突变的患者;对于仅具有高 AFB1-赖氨酸加合物水平的那些,分别为 4.26 (1.16–15.38)。对于具有 1753V 突变和高 AFB1-赖氨酸加合物水平的受试者,调整后的 OR 为 5.13 (1.79–14.71);仅具有 1753V 突变的患者为 1.20 (0.47–3.08),AFB1-赖氨酸加合物水平较高的患者则为 2.28 (1.01–5.31)。这些数据证实了 BCP 突变与 HCC 风险之间的关联,以及 1762T/1764A 双突变和 1753V 突变与这一 HCC 高风险区域中膳食 AFB1 暴露的累加效应。
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 B1 (AFB1) exposure in the formation of HCC in this high-risk area. The study recruited 60 HCC patients and 120 age-, gender-, residency-matched controls. HBV genotype and basic core promoter (BCP) mutations were determined by nested-PCR/direct sequencing. Serum AFB1-lysine adduct was measured by high performance liquid chromatography-fluorescence detection. HBV Genotype C was predominant in 75.0% of cases and 84.2% of controls. The 1762T/1764A double mutations, 1753V mutations, and 1752V 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 1762T/1764A double mutations and high AFB1-lysine adduct level; 2.01 (0.24–14.29), for those with only 1762T/1764A double mutations; and 4.26 (1.16–15.38) for those with only high AFB1-lysine adduct level, respectively. The adjusted OR was 5.13 (1.79–14.71) for subjects with 1753V mutations and high AFB1-lysine adduct level; 1.20 (0.47–3.08) for those with only 1753V mutations, and 2.28 (1.01–5.31) for those with high AFB1-lysine adduct level, respectively. These data confirmed the association of BCP mutations with HCC risk and the additive effects of 1762T/1764A double mutations and 1753V mutations with dietary AFB1 exposure in this high-risk area for HCC.
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发表时间: 2004-12-01
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发表时间: 2009-09-01
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