cigarette smoking and p16ink4α gene promoter hypermethylation in non-small cell lung carcinoma patients a meta-analysis吸烟和p16ink4α基因启动子甲基化在非小细胞肺癌患者一个荟萃分析.pdfVIP

Cigarette Smoking and p16INK4a Gene Promoter Hypermethylation in Non-Small Cell Lung Carcinoma Patients: A Meta-Analysis 1. 2. 1 3,4,5 3 1 1 Bo Zhang , Wei Zhu , Ping Yang , Tao Liu , Mei Jiang , Zhi-Ni He , Shi-Xin Zhang , Wei-Qing 3 1 Chen *, Wen Chen * 1 Department of Toxicology, Guangdong Provincial Key Laboratory of Food, Nutrition and Health, School of Public Health, Sun Yat-sen University, Guangzhou, China, 2 Department of Toxicology, Guangzhou Center for Disease Control and Prevention, Guangzhou, China, 3 Faculty of Biostatistics and Epidemiology, School of Public Health, Sun Yat-sen University, Guangzhou, China, 4 Guangdong Institute of Public Health, Guangzhou, China, 5 Center for Disease Control and Prevention of Guangdong Province, Guangzhou, China Abstract Background: Aberrant methylation of promoter DNA and transcriptional repression of specific tumor suppressor genes play an important role in carcinogenesis. Recently, many studies have investigated the association between cigarette smoking and p16INK4a gene hypermethylation in lung cancer, but could not reach a unanimous conclusion. Methods and Findings: Nineteen cross-sectional studies on the association between cigarette smoking and p16INK4a methylation in surgically resected tumor tissues from non-small cell lung carcinoma (NSCLC) patients were identified in PubMed database until June 2011. For each study, a 2 62 cross-table was extracted. In total, 2,037 smoker and 765 nonsmoker patients were pooled with a fixed-effects model weighting for the inverse of the variance. Overall, the frequency of p16INK4a hypermethylation was higher in NSCLC patients with smokin