Hu Zhuo-ying, Tang Liang-dan, Zhou Qin, Xiao Lin, Cao Yi
Department of Obstetrics and Gynecology, The First Affiliated Hospital, Chongqing Medical University, 1 Youyi Road, Chongqing, 400016, China.
Tumour Biol. 2015 Mar;36(3):1487-91. doi: 10.1007/s13277-014-2632-3. Epub 2015 Jan 17.
Previous studies demonstrated that the loss of function of the p16INK4A gene is mainly caused by the hypermethylation of p16 gene promoter; however, whether or not it is associated with the incidence of endometrial carcinoma (EC) remains unclear. In the current study, we conducted a meta-analysis to investigate the effects of p16 gene promoter hypermethylation on the incidence of EC. Detailed research publications were searched from Embase, PubMed, and ISI Web of Knowledge for composition in English or Chinese. The pooled data were collected and analyzed by Review Manager 5.2. Odds ratios (ORs) were calculated and summarized respectively. Six eligible studies, including 261 patients were selected and analyzed. The pooled OR was 0.42, test for overall effect, Z = 10.19, P < 0.0001, indicating that p16 gene promoter hypermethylation was significantly correlated with the EC patients. The results of our study strongly suggest that p16 gene promoter hypermethylation is correlated with an increased risk of EC. P16 gene promoter hypermethylation plays a critical role in endometrial carcinogenesis.
以往研究表明，p16INK4A基因功能缺失主要由p16基因启动子的高甲基化所致；然而，其是否与子宫内膜癌（EC）的发病相关仍不清楚。在本研究中，我们进行了一项荟萃分析，以探讨p16基因启动子高甲基化对EC发病的影响。从Embase、PubMed和ISI Web of Knowledge中检索了详细的研究出版物，以查找英文或中文文献。通过Review Manager 5.2收集并分析汇总数据。分别计算并汇总比值比（OR）。选择并分析了6项符合条件的研究，包括261例患者。汇总OR为0.42，总体效应检验Z = 10.19，P < 0.0001，表明p16基因启动子高甲基化与EC患者显著相关。我们的研究结果强烈表明，p16基因启动子高甲基化与EC风险增加相关。P16基因启动子高甲基化在子宫内膜癌发生中起关键作用。
