锰超氧化物歧化酶基因多态性与前列腺癌、食管癌及肺癌易感性关系的Meta分析

Associations of manganese superoxide dismutase genetic polymorphism with the susceptibilities of prostate,esophageal and lung cancers:a Meta-analysis

目的:评价锰超氧化物歧化酶(manganese superoxide dismutase,MnSOD)基因多态性与前列腺癌、食管癌及肺癌易感性的关系。方法:计算机检索Cochrane Library和PubMed等数据库,并辅以手工检索,按照纳入与排除标准选择病例-对照研究。评价质量及提取资料后,采用STATA11.0软件对数据进行Meta分析。结果:共纳入22个病例-对照研究,其中病例组8181例,健康对照组11844例。对于前列腺癌,共纳入12个病例-对照研究,其中患者4182例,健康对照6885例,Meta分析结果显示MnSOD基因多态性明显增加了前列腺癌的发病风险[杂合子模型:比值比(odds ratio,OR)=1.11,95%可信区间(confidence interval,CI)=1.01～1.22;纯合子模型:OR=1.25,95%CI=1.03～1.51;显性模型:OR=1.15,95%CI=1.01～1.31)。对于食管癌,共纳入4个病例-对照研究,其中患者620例,健康对照909例,Meta分析结果显示MnSOD基因多态性亦明显增加其发病风险(杂合子模型:OR=1.58,95%CI=1.22～2.04;纯合子模型:OR=2.25,95%CI=1.61～3.15;隐性模型:OR=1.69,95%CI=1.07～2.67;显性模型:OR=1.74,95%CI=1.36～2.22)。然而,对于肺癌,共纳入6个病例-对照研究,其中患者3375例,健康对照4050例,Meta分析结果显示MnSOD基因多态性明显降低了肺癌的发病风险(纯合子模型:OR=0.68,95%CI=0.59～0.78;隐性模型:OR=0.71,95%CI=0.54～0.93;显性模型:OR=0.83,95%CI=0.75～0.92)。结论:MnSOD基因多态性可增加前列腺癌和食管癌的发病风险,但降低肺癌的发病风险。

Objective： To evaluate the associations of manganese superoxide dismutase （MnSOD） genetic polymorphism with the susceptibilities of prostate, esophageal and lung cancers. Methods： Studies were identified by searching computerized databases （Cochrane Library, PubMed, etc.）, accompanied by manual search. The case-control studies were selected according to defined inclusion and exclusion criteria. After quality evaluation and data abstraction, a meta-analysis was performed by using STATA 11.0 software. Results： A total of 22 case-control studies were eligible for this analysis, including 8 1 81 cases and 11 844 healthy controls. For prostate cancer, 12 case-control studies included 4 182 cases and 6 885 healthy controls. Meta-analysis showed that MnSOD polymorphism could significantly increase the risk of prostate cancer [heterozygote genotype： odds ratio （OR）=1.11, 95% confidence interval （C/）=1.01-1.22; homozygote genotype： 0R=1.25, 95%C/=1.03-1.51）; dominant genotype： OR= 1.15, 95%C/=1.01-1.31）]. For esophageal cancer, 4 case-control studies contained 620 cases and 909healthy controls. Meta-analysis showed that MnSOD polymorphism could significantly increase the risk of esophageal cancer [heterozygote genotype： 0R=1.58, 95%C/=1.22-2.04; homozygote genotype： OR= 2.25, 95%C/=1.61-3.15）; recessive genotype： 0R=1.69, 95%C/=1.07-2.67）; dominant genotype： OR= 1.74, 95%C/=1.36-2.22）]. For lung cancer, 6 case-control studies contained 3 375 cases and 4 050 healthy controls. Meta-analysis showed that MnSOD polymorphism could significantly decrease the risk of lung cancer [homozygote genotype： OR=0.68, 95%C/=0.59-0.78）; recessive genotype： OR= 0.71, 95%C/=0.54-0.93）; dominant genotype： OR=0.83, 95%C/=0.75-0.92）]. Conclusion： MnSOD polymorphism is associated with elevated risks of prostate and esophageal cancers, but decreased risk of lung cancer.