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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 CYP1A1 gene polymorphism and the susceptibility to lung cancer and the effect of p16 methylation on the incidence of lung cancer. Methods Forty-seven patients with primary lung cancer and 94 patients without the same respiratory system disease and no same cancer of the same period were enrolled in this study. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and methylation Specific PCR (methylation-specific PCR, MSP) and other technologies to detect CYP1A1 gene polymorphism and p16 gene methylation. Results There was no significant difference in the distribution of CYP1A1 between lung cancer group and control group (P> 0.05). There was no obvious synergistic effect between smoking and CYP1A1 (P> 0.05). The positive rates of p16 methylation in lung cancer tissues and normal lung tissues were 44.7% (21/47) and 17.0% (8/47), respectively. The difference was significant (P <0.05). Conclusion CYP1A1 gene polymorphism does not increase the risk of lung cancer. The relationship between p16 methylation and lung cancer is very close, but there is no significant correlation between p16 methylation and CYP1A1 gene polymorphism.