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

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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 association of manganese superoxide dismutase (MnSOD) gene polymorphisms with susceptibility to prostate cancer, esophageal cancer and lung cancer. METHODS: Databases such as the Cochrane Library and PubMed were searched by computer, supplemented by manual retrieval, and case-control studies were selected according to inclusion and exclusion criteria. After evaluating the quality and extracting the data, the data was analyzed by Meta-analysis using STATA11.0 software. Results: A total of 22 case-control studies were included, of which 8,181 were case group and 11844 were healthy control group. For prostate cancer, a total of 12 case-control studies were included, including 4182 patients and 6885 healthy controls. Meta-analysis showed that MnSOD gene polymorphisms significantly increased the risk of prostate cancer [heterozygous model: odds ratio , OR) = 1.11, 95% confidence interval (CI) = 1.01-1.22; homozygous model: OR = 1.25,95% CI = 1.03-1.51; dominant model: OR = 1.15, 95% CI = 1.01 ~ 1.31). For esophageal cancer, a total of 4 case-control studies were included, including 620 patients and 909 healthy controls. Meta-analysis showed that MnSOD gene polymorphisms also significantly increased the risk of developing the disease (heterozygous model: OR = 1.58, 95% CI = 1.22-2.04; OR = 2.25, 95% CI = 1.61-3.15; Hidden model: OR = 1.69, 95% CI = 1.07-2.67; Dominant model: OR = 1.74, 95% CI = 1.36 ~ 2.22). However, a total of 6 case-control studies were included in the study, including 3375 patients and 4050 healthy controls. Meta-analysis showed that MnSOD gene polymorphisms significantly reduced the risk of lung cancer (homozygous model: OR = 0.68, 95 % CI = 0.59-0.78; Recessive model: OR = 0.71, 95% CI = 0.54-0.93; Dominant model: OR = 0.83, 95% CI = 0.75-0.92). Conclusion: MnSOD gene polymorphism can increase the risk of prostate cancer and esophageal cancer, but reduce the risk of lung cancer.
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