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Meta-analysis of the association between APC promoter methylation and colorectal cancer

机译:荟萃分析APC启动子甲基化与结直肠癌之间的关系

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摘要

Previous studies investigating the association between adenomatous polyposis coli (APC) gene promoter methylation and colorectal cancer (CRC) have yielded conflicting results. The aim of this study was to comprehensively evaluate the potential application of the detection of APC promoter methylation to the prevention and treatment of CRC. PubMed, Embase, and MEDLINE (results updated to October 2014) were searched for relevant studies. The effect size was defined as the weighted odds ratio (OR), which was calculated using either the fixed-effects or random-effects model. Prespecified subgroup and sensitivity analyses were conducted to evaluate potential heterogeneity among the included studies. Nineteen studies comprising 2,426 participants were selected for our meta-analysis. The pooled results of nine studies comprising a total of 740 subjects indicated that APC promoter methylation was significantly associated with CRC risk (pooled OR 5.53; 95% confidence interval [CI] 3.50–8.76; P<0.01). Eleven studies with a total of 1,219 patients evaluated the association between APC promoter methylation and the presence of CRC metastasis, and the pooled OR was 0.80 (95% CI 0.44–1.46; P=0.47). A meta-analysis conducted with four studies with a total of 467 patients found no significant correlation between APC promoter methylation and the presence of colorectal adenoma (pooled OR 1.85; 95% CI 0.67–5.10; P=0.23). No significant correlation between APC promoter methylation and patients’ Dukes’ stage, TNM stage, differentiation grade, age, or sex was identified. In conclusion, APC promoter methylation was found to be significantly associated with a higher risk of developing CRC. The findings indicate that APC promoter methylation may be a potential biomarker for the carcinogenesis of CRC.
机译:先前研究腺瘤性息肉病(APC)基因启动子甲基化与结直肠癌(CRC)之间的关联的研究得出了相互矛盾的结果。这项研究的目的是全面评估APC启动子甲基化检测在预防和治疗CRC中的潜在应用。搜索PubMed,Embase和MEDLINE(结果更新至2014年10月)以进行相关研究。效应大小定义为加权比值比(OR),可使用固定效应模型或随机效应模型计算得出。进行了预先指定的亚组和敏感性分析,以评估纳入研究之间的潜在异质性。我们选择了19个研究,其中包括2,426名参与者,进行了荟萃分析。总共740名受试者的9项研究的汇总结果表明,APC启动子甲基化与CRC风险显着相关(合并OR 5.53; 95%置信区间[CI] 3.50-8.76; P <0.01)。总共1219例患者的11项研究评估了APC启动子甲基化与CRC转移存在之间的相关性,合并OR为0.80(95%CI 0.44-1.46; P = 0.47)。对总共467例患者进行的四项研究的荟萃分析发现,APC启动子甲基化与结直肠腺瘤的存在之间无显着相关性(合并OR 1.85; 95%CI 0.67-5.10; P = 0.23)。没有发现APC启动子甲基化与患者的Dukes分期,TNM分期,分化程度,年龄或性别之间存在显着相关性。总之,发现APC启动子甲基化与发生CRC的较高风险显着相关。这些发现表明,APC启动子甲基化可能是CRC致癌的潜在生物标记。

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