摘要
目的分析非小细胞肺癌(NSCLC)及癌周正常肺组织p16基因甲基化改变及p16蛋白表达情况。 方法选取各种病理类型的非小细胞肺癌(NSCLC)标本共40例作为研究对象,同时选取癌组织周围的正常肺组织作为对照。运用甲基化特异性PCR(MSP)方法检测肺癌标本及周围正常肺组织中p16基因的甲基化改变情况,运用免疫组化方法检测p16蛋白在肺癌标本及周围正常肺组织中的表达情况。 结果①40例肺癌标本中,29例发生了p16基因甲基化。而其周围正常肺组织只有5例发生了p16基因甲基化。二者有明显差异(P<0.01)。②40例肺癌标本中,26例p16蛋白表达降低,而其周围正常肺组织只有5例蛋白表达降低,二者有明显差异(P<0.01)。③29例p16基因发生了甲基化改变的肺癌标本中,有22例发生了p16蛋白表达降低。在11例未发生p16基因甲基化改变的肺癌标本中,有4例发生了p16蛋白表达降低。 结论p16基因甲基化是导致非小细胞肺癌(NSCLC)p16蛋白表达降低的重要机制。
Objective To study p16 methylation and p16 protein expression in Non-Small Cell lung Cancers(NSCLC). Methods 40 NSCLC and its surrounding normal lung tissure were chosed to study the p16 methylation status and p16 protein expression with the method of MSP (methylation-specificPCR) and immunohistochemistry. Results ① Among 40 NSCLC, p16 methylation were found in 29 patients. In contrast, p16 methylation were found in only 5 of their surrounding normal lung tissue (P< 0. 01). ② 26 of 40 NSCLC showed lower p16 protein expression. In contrast,only 8 of their surrounding normal lung tissue showed lower p16 protein expression (P<0. 01). ③ Among 29 NSCLC with p16 methylation, 22 were found lower p16 protein expression. Among 11 NSCLC without p16 methylation, 4 were found lower p16 protein expression. Conclusion p16 methylation is the main cause of lower p16 protein expression in NSCLC.
出处
《空军总医院学报》
2004年第1期25-27,30,共4页
Journal of General Hospital of Air Force,PLA