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目的:研究脑胶质瘤中p16基因启动子区甲基化情况及其临床意义。方法:用甲基化特异性PCR技术检测42例脑胶质瘤组织和癌旁正常脑组织中p16基因启动子甲基化,并分析该基因启动子甲基化与临床病理特征之间的关系。结果:脑胶质瘤组织中p16基因异常甲基化率(38.27%)显著高于癌旁正常脑组织中p16基因的异常甲基化率(8.8%,P=0.000)。发生甲基化的肿瘤组织或者正常脑组织中p16基因mRNA和蛋白表达显著降低。此外,p16基因异常甲基化和肿瘤病理分级有相关性(P=0.007),而与患者性别、年龄及肿瘤类型等临床特征无关(P=0.669,0.869和0.944)。结论:p16基因启动子区CpG岛高甲基化与p16表达下调相关,推测p16启动子区CpG岛高甲基化是导致p16基因在脑胶质瘤中表达下调的重要因素,有望成为脑胶质瘤早期辅助诊断的分子标志物之一。
Objective: To study the methylation status of p16 gene promoter in glioma and its clinical significance. Methods: The methylation of promoter of p16 gene in 42 glioma tissues and adjacent normal brain tissues was detected by methylation-specific PCR. The relationship between promoter methylation and clinicopathological features was analyzed . Results: The abnormal methylation rate of p16 gene (38.27%) in glioma tissues was significantly higher than that in adjacent normal tissues (8.8%, P = 0.000). The methylation of tumor tissue or normal brain tissue p16 gene mRNA and protein expression was significantly reduced. In addition, abnormal methylation of p16 gene was correlated with tumor grade (P = 0.007), but not with clinical features such as gender, age and tumor type (P = 0.669, 0.869 and 0.944). Conclusion: The hypermethylation of CpG island in promoter region of p16 gene is correlated with the down-regulation of p16 expression. It is speculated that hypermethylation of CpG island in p16 promoter is an important factor that leads to the down-regulation of p16 gene in glioma. One of the molecular markers of diagnosis.