脑胶质瘤中pRb表达与CDK_4、MTS基因异常的相关性研究  

Molecular pathological study on expression of pRb and CDK 4,MTS gene changes in human gliomas

作　　者：田新华[1] 江澄川[1] 高翔[1] 陈商群[1] 许凯黎[1,2] 周瑾[1,2] 

机构地区：[1]上海华山医院神经外科 [2]上海市肿瘤研究所

出　　处：《中华神经外科杂志》2001年第1期14-16,共3页Chinese Journal of Neurosurgery

基　　金：国家教委博士点基金资助项目(96026515)

摘　　要：目的　探讨脑胶质瘤中CDK4 、MTS基因异常及pRb表达改变与脑胶质瘤发生发展的相关性。方法　应用PCR SSCP、分子杂交及免疫组化技术检测 6 8例不同病理分级脑胶质瘤。结果　p16基因表达阴性或pRb无表达或CDK4 扩增多为单独发生 ,其中III IV级肿瘤中pRb、p16蛋白失表达或p15基因缺失或CDK4 基因扩增的综合发生率为 89% (4 2 / 47)。结论　脑胶质瘤中细胞生长周期“关卡”蛋白p16、pRb、或CDK4 单因素的异常比交错并发的改变更为常见 ,p16、pRb失活或CDK4 扩增的任一改变 ,即可能破坏细胞增殖的正常调控 。Objective To investigate expression of pRb and CDK 4, MTS gene changes in human gliomas and relationship with the clinical pathology. Methods Brain gliomas with different pathologic types were detected by using PCR SSCP, Southern blot, Slot blot and immunohistochemistry. Results The negative expression of p16 or pRb and CDK 4 amplification often occurred independently. The total rate of negative expression of p16 and/or pRb and/or deletion of p15 and/or CDK 4 amplification were in 89% (42/47).Conclusions The propensity was occurrence of singular (89%) rather than combined aberrant expression of p16 or pRb or CDK 4 amplification. The suppression of p16, p15 or pRb or the increased activity of CDK 4 were sufficient to disrupt this regulatory mechanism in a manner that favors cell proliferation and tissues canceration.

关 键 词：脑胶质瘤 RB蛋白 MTS基因 CDK4基因 分子杂交 基因异常 

分 类 号：R739.41[医药卫生—肿瘤]