【作者】 金永堂； 汪亚松； 徐迎春； 薛绍礼； 于在诚； 刘晓； 田敏华； 陶文虎； 孔云明； 侯勇；

【机构】 浙江大学公共卫生学院； 安徽医科大学公共卫生学院； 安徽医科大学第一附属医院胸外科； 安徽省合肥市第一人民医院体检中心；

【摘要】 目的:研究P16基因甲基化在非小细胞肺癌发病过程中的作用及其影响因素,为探索肺癌发病机制提供依据。方法:采用甲基化特异性PCR(MSP)技术检测47例非小细胞肺癌患者肺癌组织和47例对应癌旁组织中DNA的P16基因甲基化状况,同时收集吸烟等环境暴露资料。结果:肺癌组织中P16基因甲基化率44．7％,高于癌旁组织的17％(P<0．01),P16 基因甲基化好发于鳞癌(P<0．05),在鳞癌中肺癌组织P16基因甲基化率明显高于癌旁组织,对比有统计学意义(P<0．01), 且P16甲基化和吸烟在鳞癌中高度相关(P<0．01)。结论:P16基因甲基化可能参与鳞癌的形成,且与吸烟高度相关。更多还原

【Abstract】 Objective: To study the effect of P16 gene methylation in non - small cell lung cancer and correlative factors so as to explore the mechanism of lung cancer. Methods: The MSP method was introduced to test the methylation status of DNA from 47 lung cancer tissues and corresponding nonmalignant tissues, meanwhile data of environment exposure such as smoking. was collected . Results: The total frequency of pl6 methylation was 44.7% in lung cancer tissues, significantly higher than that in the nomalignant tissues 17%(P < 0.01). P16 methylation significantly was more seen in squamous cell carcinomas( P < 0.05), there was a statistic difference of methylation frequency between lung cancer tissues and nonmalignant tissues in squamous cell carcinomas( P < 0.01), and methylation significantly correlated with smoking in squamous cell carcinomas( P < 0.01). Conclusion: It was demonstrated that methylation of P16 gene owing to smoking maybe involved in the progress of squamous cell carcinomas.更多还原