The State Key Laboratory of Genetic Engineering, Fudan University, 200433, Shanghai, China.
Med Oncol. 2011 Dec;28(4):1129-35. doi: 10.1007/s12032-010-9597-x. Epub 2010 Jun 15.
Studies investigating the relationship between TP53 Arg72Pro polymorphism and endometrial cancer risk reported conflicting results. To explore a more precise estimate of the effect of this polymorphism on endometrial carcinogenesis, a meta-analysis was performed by searching eligible studies in PubMed. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the association for codominant model (Arg/Arg vs. Pro/Pro, Arg/Pro vs. Pro/Pro), dominant model (Arg/Arg+Arg/Pro vs. Pro/Pro), and recessive model (Arg/Arg vs. Arg/Pro+Pro/Pro), respectively. Subgroup analyses were performed by Hardy-Weinberg equilibrium (HWE) in controls, the specimen of cases for determining TP53 genotypes, sample size, the source of control and case groups, and ethnicity. We identified 8 case-control studies involving 2,154 subjects for this meta-analysis. Overall, no evidence of association was observed between TP53 genotypes and endometrial cancer risk in all genetic models (Arg/Arg vs. Pro/Pro: OR=0.98, 95% CI: 0.69-1.39, P=0.90; Arg/Pro vs. Pro/Pro: OR=1.00, 95% CI: 0.71-1.42, P=0.98; dominant model: OR=0.99, 95% CI: 0.71-1.38, P=0.95; recessive model: OR=1.06, 95% CI: 0.80-1.41, P=0.95). Stratified analyses also detected no significant association in any subgroup, except among those studies with controls deviated from HWE in recessive model (OR=1.60, 95% CI: 1.07-2.39). In conclusion, we did not observe any evidence for a role of TP53 Arg72Pro polymorphism in endometrial cancer. The reported significant association between this polymorphism and endometrial cancer risk may be due to methodological errors such as selection bias, small sample size, Type I error, and population stratification.
研究探讨了 TP53 Arg72Pro 多态性与子宫内膜癌风险之间的关系，结果相互矛盾。为了更准确地评估这种多态性对子宫内膜癌变的影响，我们通过在 PubMed 中搜索合格的研究进行了荟萃分析。使用粗odds ratios（ORs）和 95%置信区间（CIs）来评估共显性模型（Arg/Arg 与 Pro/Pro、Arg/Pro 与 Pro/Pro）、显性模型（Arg/Arg+Arg/Pro 与 Pro/Pro）和隐性模型（Arg/Arg 与 Arg/Pro+Pro/Pro）的相关性。根据 Hardy-Weinberg 平衡（HWE）在对照组、确定 TP53 基因型的病例标本、样本量、对照组和病例组的来源以及种族进行亚组分析。我们确定了 8 项病例对照研究，涉及 2154 名受试者进行荟萃分析。总体而言，在所有遗传模型中，TP53 基因型与子宫内膜癌风险之间均未观察到相关性（Arg/Arg 与 Pro/Pro：OR=0.98，95%CI：0.69-1.39，P=0.90；Arg/Pro 与 Pro/Pro：OR=1.00，95%CI：0.71-1.42，P=0.98；显性模型：OR=0.99，95%CI：0.71-1.38，P=0.95；隐性模型：OR=1.06，95%CI：0.80-1.41，P=0.95）。分层分析也没有在任何亚组中检测到显著相关性，除了在隐性模型中对照组偏离 HWE 的研究（OR=1.60，95%CI：1.07-2.39）。总之，我们没有观察到 TP53 Arg72Pro 多态性在子宫内膜癌中的作用证据。报道的这种多态性与子宫内膜癌风险之间的显著相关性可能是由于方法学错误，如选择偏倚、样本量小、I 型错误和群体分层。
