摘要
目的探讨p16基因甲基化对非小细胞肺癌发病的影响。方法原发性肺癌患者47例及同期无呼吸系统疾病又未患任何肿瘤同性别者94例作对照,采用甲基化特异性PCR等技术,检测p16基因甲基化。结果p16基因甲基化在肺癌组织和正常肺组织中检出率分别为44.7%(21/47)和17.0%(8/47),两者有显著差异(P<0.05)。37例非小细胞肺癌吸烟者中有21例肺癌组织发生p16基因甲基化,而10例非小细胞肺癌非吸烟者中无一例肺癌组织发生p16基因甲基化。p16基因甲基化与年龄、饮酒、肺癌病理分型及肺癌临床分期之间均无明显的相关性(P>0.05)。结论p16基因甲基化与非小细胞肺癌发生的关系非常密切,p16基因甲基化与吸烟有关。检测p16基因甲基化与否,可能有助于肺癌的诊断。
Objective To study the effects of the methylation in p16 gene on the risk of non - small cell lung cancer. Methods A case control study was conducted among 47 cases of lung cancer and 94 controls.A methylation- specific PCR was performed to detect p16 methylation. Results Methylated p16 gene was found in 44.7% （21/47） of lung cancer tissues and in 17.0% （8/47） of normal lung tissues with significant difference （P 〈 0. 05）. 21 of 37 non - small cell lung cancer tissues of smokers showed methylation of the p16, while none of 10 non - small cell lung cancer tissues of non - smokers showed methylation of the p16. The methylation in p16 gene is not significantly associated with age, alcohol drinking, histologic type and stage of non - small cell lung cancer （P 〉 0.05 ）. Conclusion The genetic polymorphism of CYP1A1 does not increase the risk of lung cancer. The methylation in p16 gene is strongly associated with lung cancer and is associated with tobacco smoking. Examining the methylation status of the p16 gene might be useful for the diagnosis of lung cancer.
出处
《癌症进展》
2007年第4期393-397,403,共6页
Oncology Progress
基金
国家自然科学基金资助项目(NO.30471427)
