摘要
目的:进一步探讨结肠腺瘤性息肉病基因(APC基因)的失活在卵巢癌的发生、发展中的作用。方法:搜索PubMed、EMBase、Web of Science及CNKI数据库中2000年1月1日—2014年12月31日有关APC基因甲基化与卵巢上皮癌相关的文献,纳入研究均为包含病例组及对照组的随机对照试验。纳入文献采用纽卡斯尔-渥太华量表(NOS)评价标准。使用Stata 11.0软件进行OR值、异质性及发表性偏倚的相关的统计学分析。结果:共纳入9篇文献,其中包括641例卵巢癌患者和377例对照者。总病例组与总对照组的APC基因甲基化发生率差异有统计学意义(OR=6.19,95%CI:4.08~9.41,P=0.000);卵巢癌组织与正常组织的APC基因甲基化发生率差异有统计学意义(OR=5.88,95%CI:3.66~9.45,P=0.000);卵巢癌组织与良性卵巢肿瘤组织的APC基因甲基化发生率差异有统计学意义(OR=6.99,95%CI:3.12~15.64,P=0.000)。结论:APC基因甲基化可能与卵巢癌有关。
Objective:To investigate the role of APC gene inactivation in the occurrence and development of ovarian cancer. Methods:Databases such as Pub Med, EMBase, Web of Science, and CNKI data were searched. Related literatures were published from January 1, 2000 to December 31, 2014. Only randomized controlled trials were included. The quality of the included studies were assessed by Newcastle-Ottawa Scale(NOS). Stata 11.0 software was used for statistical analysis such as OR value,heterogeneity and publication bias. Results:Nine studies, with 641 ovarian cancer patients and 377 controls were included in the Meta-analysis. Statistical results shows that the pooled odds ratio was 6.19(95% CI: 4.08-9.41, P=0.000) in the case group versus the control group under fix effects model. The pooled odds ratio was 5.88(95%CI: 3.662-9.450, P=0.000) in the cancer group versus the normal group under fix effects model. The pooled odds ratio was 6.99(95% CI: 3.12-15.64, P =0.000) in the cancer group versus the benign tumor group under fix effects model. Conclusions:This analysis suggests that APC gene methylation had an association with ovarian cancer.
出处
《国际妇产科学杂志》
CAS
2016年第2期169-173,共5页
Journal of International Obstetrics and Gynecology
基金
教育部高校博士学科点专项基金(20124503110003)
广西科学研究与技术开发计划项目(桂科攻1140003A-34)