【摘要】 背景与目的:探讨FHIT和p16基因甲基化与肺癌发生之间的关系。材料与方法:采用甲基化特异性PCR检测59例原发性肺癌组织,相对应的32例正常组织及11例支气管鳞状化生组织中FHIT基因、p16基因启动子区CpG岛甲基化状况。结果:肺癌组织和正常肺组织中的FHIT基因甲基化率分别为37.3%(22/59)、0.0%(0/32),两组间的差异有统计学意义(P<0.01);支气管鳞状化生组织FHIT基因甲基化阳性率为18.1%(2/11)。肺癌组织和正常肺组织中的p16基因甲基化率分别为50.8%(30/59)、0.0%(0/32),两组间的差异具有统计学意义(P<0.01);支气管鳞状化生组织p16基因甲基化阳性率为18.1%(2/11)。肺癌患者吸烟组中FHIT、p16基因甲基化联合检测的阳性率为90.6%(29/32),与非吸烟组(33.3%,9/27)相比较,其差异具有统计学意义(P<0.05)。结论:FHIT基因和p16基因启动子区甲基化可能与肺癌的发生有关。更多还原

【Abstract】 BACKGROUND AND AIM: To illustrate the relationship between the methylation of FHIT and p16 genes and the development of lung cancer.MATERIALS AND METHODS: Methylation of the promoters of FHIT gene and p16 gene was evaluated by methylation-specific PCR in 59 lung cancer tissues,32 adjacent non-carcinoma tissues and 11 bronchal epithelial squamous tissues.RESULTS: FHIT methylation in lung cancer tissue samples,adjacent non-carcinoma tissue samples were 37.3%(22/59) and 0%(0/32)respectively,with significant difference(P<0.01).Methylation was found in 2 of 11(18.1%) bronchal epithelial squamous samples.p16 methylation of lung cancer tissue samples,adjacent non-carcinoma tissue samples were 50.8%(30/59)and 0.0%(0/32)respectively,showing a significant difference(P<0.01);Methylation was found in 2(18.1%)of 11 bronchal epithelial squamous samples.FHIT/p16 combined detection of methylation found many more positive tissues in smoking patients than the single gene.There was a significant difference between smokers and non-smokers(P<0.05).CONCLUSION: The 5’-CpG island methylation of FHIT and p16 was frequent in lung cancer and may be an early event in lung carcinogenesis.更多还原