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。
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.
出处
《癌变·畸变·突变》
CAS
CSCD
2009年第4期291-294,共4页
Carcinogenesis,Teratogenesis & Mutagenesis
基金
国家自然科学基金资助项目(30872095)
