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目的 研究非小细胞肺癌(non-smal celllung cancer,NSCLC)患者p16、DAPK和RARβ启动子区CpG岛甲基化对临床特征的影响,探讨其与吸烟的关系.方法 应用甲基化特异性PCR检测200例原发性NSCLC组织和相应正常组织中p16,DAPK和RARβ基因启动子区CpG岛甲基化状况.结果 p16、DAPK和RARβ基因甲基化在癌组织中的检出率分别为51.0%、60.0%和58.0%,均高于其在正常组织中的检出率(分别为12.5%,11.5%和15.0%;P<0.05).非条件Logistic回归显示,癌组织p16基因甲基化与年龄和病例组织类型有关(P<0.05);癌组织DAPK基因甲基化与年龄、性别、临床分类有关(P<0.05);而癌组织RARβ基因甲基化与临床分类和TNM(tumor node metastasis)分期相关(P<0.05).癌组织p16基因甲基化与DAPK基因甲基化之间存在交互作用(OR=1.987,95%CI:1.055~3.743).吸烟者癌组织p16和DAPK基因甲基化的OR值分别为3.139(95%CI:1.046~9.419)和3.585(95%CI:1.270~10.123),未发现癌组织RARβ基因甲基化与吸烟有关.结论 p16,DAPK和RARβ甲基化与NSCIC患者临床特征关系密切.吸烟与p16和DAPK基因甲基化有关.Abstract: Objective To investigate the effects of promoter methylation of p16 , death-associated protein kinase (DAPK) and retinoic acid receptor-β (RARβ) genes on clinical data in non-small cell lung cancers, and to study the effect of smoking on the risk of gene methylation. Methods The promoter methylation of p16 , DAPK and RARβ genes in 200 primary non-small cell lung cancers and the corresponding nonmalignant lung tissues were determined by methylation-specific PCR. Results Methylation in the tumor tissues was detected in 51.0% for p16 , 60.0% for DAPK, and 58. 0% for RARβ gene, with significant differences (P < 0. 05) when compared with those in the corresponding nonmalignant tissues (12. 5%,11.5% and 15.0%) respectively. p16 gene methylation in tumor tissue was associated with age significantly in unconditional logistic regression analysis (P<0.01) and histologic type (P<0. 05). DAPK gene methylation in tumor tissue was associated significantly with age (P<0. 05), gender (P<0.05) and clinical type (P< 0.05 ). RARβ gene methylation in tumor tissue was associated with clinical type (P<0. 05) and tumor stage (P<0. 05) significantly. The interaction odds ratio (OR) for the gene-gene interaction in tumor tissue between p16 and DAPK was 1. 987 (95%CI: 1. 055-3. 743). The results of the gene-smoking analyses revealed that a relationship existed between cigarette smoking and p16 gene methylation (OR= 3. 139, 95 % CI: 1. 046-9. 419), the OR for the relationship of DAPK gene methylation and cigarette smoking was 3. 585(95%CI: 1. 270-10. 123)in tumor tissue. The RARβ gene methylation did not differ based on the smoking status of patients in tumor tissue. Conclusion Thep16 , DAPK and RARβ genes methylation are strongly associated with clinical data of non-small cell lung cancer, and methylation of p16 and DAPK genes are associated with tobacco smoking. 相似文献
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