Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis.
Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis.
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DOI：
10.1093/jnci/djp180
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发表时间：
2009-08-05
期刊：
影响因子：
--
通讯作者：
Cao G
中科院分区：
文献类型：
--
作者：
Liu S;Zhang H;Gu C;Yin J;He Y;Xie J;Cao G
由于文献中相互矛盾的数据，乙肝病毒(乙肝病毒)突变和肝癌发生之间的联系仍然存在争议。我们进行了病例对照和队列研究的荟萃分析，以检查HBVPreS、增强子II(EnhII)、基本核心启动子(BCP)和前C区突变与肝细胞癌(HCC)风险的关系。我们检索了截至2008年8月31日发表的英文或中文数据库中关于这些关联的研究。使用随机效应模型合并了乙肝病毒变异的特异性优势比和相对风险，并按潜在的混杂因素进行分层。所有的统计检验都是双面的。在这项荟萃分析的43项研究中，有40项采用病例对照设计。这43项研究共评估了11名 感染的582名参与者，其中2,801人患有肝癌。Pres突变(3.77，95%可信区间=2.57~5.52)、EnhII中C1653T(2.76，95%CI=2.09~3.64)、T1753V(2.35，95%CI=1.63~3.40)和BCP中A1762T/G1764A(3.79，95%CI=2.71~5.29)对肝癌有统计学意义。在感染HBVC型的人中，PreS突变与肝癌风险的增加比在感染HBVB型的人中更强，而A1762T/G1764A的情况则相反。C1653T、T1753V和A1762T/G1764A在乙肝e抗原(HBeAg)阳性受试者中与肝癌风险增加的相关性比HBeAg阴性受试者更强。PreS突变、C1653T、T1753V和A1762T/G1764A在慢性乙肝病毒感染从无症状携带者状态发展到肝细胞癌的过程中积累(每种突变的P趋势为.001)。PreS突变、C1653T、C1653T+T1753V和基于A1762T/G1764A的突变组合对预测肝癌的特异性大于80%。前C区突变G1896A和C1858T与HBeAg状态和HBV型无关。HBVpreS突变、C1653T、T1753V和A1762T/G1764A与肝癌风险增加相关。这些突变单独和联合可能是肝癌发生的预测因素。
The association between hepatitis B virus (HBV) mutations and hepatocarcinogenesis remains controversial because of conflicting data in the literature. We conducted a meta-analysis of case–control and cohort studies to examine HBV PreS, enhancer II (EnhII), basal core promoter (BCP), and precore mutations in relation to the risk of hepatocellular carcinoma (HCC). We searched databases for studies of these associations that were published in English or Chinese up to August 31, 2008. HBV mutation–specific odds ratios and relative risks were pooled by use of a random-effects model and stratified by potential confounders. All statistical tests were two-sided. Of the 43 studies included in this meta-analysis, 40 used a case–control design. The 43 studies evaluated a total of 11 582 HBV-infected participants, of whom 2801 had HCC. Statistically significant summary odds ratios of HCC were obtained for any PreS mutation (3.77, 95% confidence interval [CI] = 2.57 to 5.52), C1653T in EnhII (2.76, 95% CI = 2.09 to 3.64), T1753V (2.35, 95% CI = 1.63 to 3.40), and A1762T/G1764A in BCP (3.79, 95% CI = 2.71 to 5.29). PreS mutations were more strongly associated with an increased risk of HCC in subjects who were infected with HBV genotype C than in those who were infected with HBV genotype B, whereas the opposite was true for A1762T/G1764A. C1653T, T1753V, and A1762T/G1764A were more strongly associated with an increased risk of HCC in hepatitis B e antigen (HBeAg)–positive subjects than in HBeAg-negative subjects. PreS mutations, C1653T, T1753V, and A1762T/G1764A accumulated during the progression of chronic HBV infection from the asymptomatic carrier state to HCC (Ptrend < .001 for each mutation). PreS mutations, C1653T, C1653T + T1753V, and A1762T/G1764A-based combinations of mutations had specificities greater than 80% for the prediction of HCC. The precore mutations G1896A and C1858T were not associated with the risk of HCC, regardless of HBeAg status and HBV genotype. HBV PreS mutations, C1653T, T1753V, and A1762T/G1764A are associated with an increased risk of HCC. These mutations alone and in combination may be predictive for hepatocarcinogenesis.
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影响因子：
120.7
作者：
Chen, CJ;Yang, HI;Iloeje, UH
通讯作者：
Iloeje, UH
影响因子：
12.7
作者：
Bläckberg, J;Kidd-Ljunggren, K
通讯作者：
Kidd-Ljunggren, K
影响因子：
5.4
作者：
Buckwold, VE;Xu, ZC;Ou, JH
通讯作者：
Ou, JH
影响因子：
11.8
作者：
Ito, K;Tanaka, Y;Mizokami, M
通讯作者：
Mizokami, M
影响因子：
2.5
作者：
Jang, J. W.;Lee, Y. C.;Yoon, S. K.
通讯作者：
Yoon, S. K.