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目的了解乙型肝炎病毒(HBV)前S基因缺失突变是否是肝癌的危险因素以及它的作用是否受HBV核心基因启动子双突变的混淆影响。方法按巢式匹配病例对照研究的方法,从隆安研究队列中选择33对病例(肝癌患者)和对照(HBsAg无症状携带者),配对的条件之一是病例和对照HBV核心基因启动子序列相同,用套式聚合酶链反应(nested PCR)对研究对象血清HBV前S基因扩增和序列分析。结果肝癌患者组前S基因缺失突变率(45.5%,15/33)显著高于对照组(6/33,18.2%)(χ2=7.364,P<0.01);男女间突变率无显著性差异(28%与43.8%,χ2=1.386,P>0.05)。多因素条件logistic回归分析结果显示,前S缺失突变是肝癌的危险因素(危险比为7,95%可信区:0.861-56.894),而HBeAg,抗-HBe及肝功能则与肝癌无关。核心基因启动子双突变组与核心基因启动子野毒株组之间的前S缺失突变率无显著性差异(χ2=0.597,P>0.05)。结论HBV前S缺失突变是肝癌的独立的危险因素,它的发生及作用与核心基因启动子双突变无关。
Objective To investigate whether the deletion of the pre-S gene of hepatitis B virus (HBV) is a risk factor for hepatocellular carcinoma (HCC) and whether its role is affected by the confusion of double mutations in HBV core promoter. Methods According to the nested matching case-control study, 33 pairs of cases (liver cancer patients) and control (HBsAg asymptomatic carriers) were selected from the Longan study cohort. One of the matching conditions was the same as the control HBV core gene promoter sequence , And the nested PCR was used to amplify and sequence the pre-HBV HBV S gene. Results The mutation rate of pre-S gene in patients with HCC was significantly higher than that of controls (45.3%, 15/33) (χ2 = 7.364, P <0.01), but there was no significant difference between male and female 28% and 43.8%, χ2 = 1.386, P> 0.05). Multivariate conditional logistic regression analysis showed that pre-S deletion mutation was a risk factor for HCC (hazard ratio: 7,95% confidence interval: 0.861-56.894), while HBeAg, anti-HBe and liver function were not associated with HCC. There was no significant difference in the rate of pre-S deletion mutation between the double-mutation group of core gene promoter and the wild-type group of core gene promoter (χ2 = 0.597, P> 0.05). Conclusion Pre-S deletion mutation of HBV is an independent risk factor of hepatocellular carcinoma, and its occurrence and role are not related to double mutation of core gene promoter.