摘要
目的探讨CYP1A1基因多态性与肺癌易感性的关系及p16基因甲基化对肺癌发病的影响。方法选取原发性肺癌患者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,采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)和甲基化特异性PCR(methylation-specificPCR,MSP)等技术,检测CYP1A1的基因多态性和p16基因甲基化。结果CYP1A1在肺癌组和对照组分布差异无统计学意义(P>0.05);吸烟与CYP1A1未见明显的协同作用(P>0.05)。p16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)、17.0%(8/47),两者差异有显著性(P<0.05)。结论CYP1A1基因多态性不增加患肺癌的危险,p16甲基化与肺癌发生的关系非常密切,但p16甲基化与CYP1A1基因多态性无明显相关性。
Objective To investigate the relationship between the genetic polymorphism of CYP1 A1 and the genetic susceptibility to lung cancer as well as to study the effects of the methylation in p16 gene on the risk of lung cancer. Methods A case control study was conducted among 47 cases of lung cancer and 94 controls. The genetic polymorphism of CYP1A1 were tested with method of PCR-RFLP, and a methylation-specific PCR was performed to detect p16 gene methylation. Results It showed that there was no significant difference in frequencies of the genotypes of CYP1A1 between the two groups（P 〉 0.05）. Synergistic effects were not found between smoking and CYP1A1. 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 differe the risk of lung cancer. Th associated with genotype of nce （P 〈 0. 05 ）. Conclusion The genetic polymorphism of CYP1 A1 does not increase e methylation in p16 gene is strongly associated with lung cancer,and is not significantly CYP1A1.
出处
《安徽医科大学学报》
CAS
北大核心
2007年第1期62-66,共5页
Acta Universitatis Medicinalis Anhui
基金
国家自然科学基金资助项目(编号:30471427)
