Genetic Association Between Angiotensinogen Polymorphisms and Lung Cancer Risk.
Genetic Association Between Angiotensinogen Polymorphisms and Lung Cancer Risk.
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DOI：
10.1097/md.0000000000001250
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发表时间：
2015-09
期刊：
影响因子：
1.6
通讯作者：
Cao Y
中科院分区：
文献类型：
--
作者：
Wang H;Zhang K;Qin H;Yang L;Zhang L;Cao Y
早期发表的研究调查血管紧张素原基因多态性与肺癌风险之间的关联，没有一致的结果。在这项研究中，我们总结了所有目前可用的数据，以检查相关性的荟萃分析。通过Embase、科克伦图书馆、ISI Web of Science（Web of Knowledge）、Google Scholar、PubMed和CNKI数据库确定了正在研究的相关性病例对照研究。肺癌风险（比值比[OR]和95%置信区间[CI]）采用固定或随机效应模型进行估计，假设所有血管紧张素原多态性均为纯合子、等位基因、杂合子、显性和隐性模型。我们在该荟萃分析中共识别出10篇文章，包括7篇Leu 84 Phe，4篇Ile 143 Val和3篇Leu 53 Leu。在Leu 84 Phe多态性的荟萃分析中，纯合子模型提供的OR为1.44（Phe/Phe vs Ile/Ile：OR = 1.44，95%CI = 1.04-1.99，异质性检验（Q检验）的P值[PHet]= 0.382）。 在隐性模型中也同样显示出显著增加的风险（Phe/Phe vs Phe/Ile + Ile/Ile：OR = 1.41，95%CI = 1.02-1.95，PHet = 0.381）。 我们还观察到在高加索亚组中存在正相关。Ile 143瓦尔多态性检测的杂合子模型和显性模型显示风险略有增加（Ile/瓦尔vs Ile/Ile：OR = 1.16，95% CI = 1.00-1.36，PHet = 0.323;瓦尔/瓦尔+Ile/瓦尔vs Ile/Ile：OR = 1.15，95% CI = 0.99-1.34，PHet = 0.253）。 这些数据表明，Leu 84 Phe和Ile 143 Val多态性在血管紧张素原基因可能是有用的生物标志物在某些特定人群中的肺癌。
Earlier published studies investigating the association between polymorphisms in the angiotensinogen gene and lung cancer risk showed no consistent results. In this study, we have summarized all currently available data to examine the correlation by meta-analysis. Case–control studies addressing the association being examined were identified through Embase, the Cochrane Library, ISI Web of Science (Web of Knowledge), Google Scholar, PubMed, and CNKI databases. Risk of lung cancer (odds ratio [OR] and 95% confidence interval [CI]) was estimated with the fixed or the random effects model assuming homozygous, allele, heterozygous, dominant, and recessive models for all angiotensinogen polymorphisms. We identified a total of 10 articles in this meta-analysis, including 7 for Leu84Phe, 4 for Ile143Val, and 3 for Leu53Leu. In the meta-analysis of Leu84Phe polymorphism, the homozygous model provided an OR of 1.44 (Phe/Phe vs Ile/Ile: OR = 1.44, 95% CI = 1.04–1.99, P values for heterogeneity test (Q-test) [PHet] = 0.382). The significantly increased risk was similarly indicated in the recessive model (Phe/Phe vs Phe/Ile + Ile/Ile: OR = 1.41, 95% CI = 1.02–1.95, PHet = 0.381). We also observed a positive association in the Caucasian subgroup. The heterozygous model and the dominant model tested for the Ile143Val polymorphism showed a marginally increased risk (Ile/Val vs Ile/Ile: OR = 1.16, 95% CI = 1.00–1.36, PHet = 0.323; Val/Val + Ile/Val vs Ile/Ile: OR = 1.15, 95% CI = 0.99–1.34, PHet = 0.253). These data suggest that Leu84Phe and Ile143Val polymorphisms in the angiotensinogen gene may be useful biomarkers for lung cancer in some specific populations.