脑肿瘤p16基因缺失、突变及5’CpG岛甲基化研究  

DELETION,MUTATION AND 5'CpG ISLAND METHYLATION OF p16 GENE IN BRAIN TUMOR

作　　者：翟广[1] 袁先厚[2] 宋来君[1] 

机构地区：[1]河南医科大学附属第一医院神经外科,郑州450052 [2]湖北医科大学附属第二医院神经外科

出　　处：《肿瘤》2001年第4期281-284,共4页Tumor

摘　　要：目的　探讨不同种类的脑肿瘤p16基因变异及其与脑肿瘤的发生、发展的关系。方法　利用PCR、PCR SSCP及PCR based甲基化技术检测了 5 6例脑胶质瘤、15例脑膜瘤及 2例原发性脑淋巴瘤p16基因缺失、突变及 5’CpG岛甲基化状况。结果　 18例高病理级别的脑胶质瘤及 1例原发性脑淋巴瘤发生p16基因缺失 ;6例脑胶质瘤及 1例原发性脑淋巴瘤发生p16基因 5’CpG岛甲基化 ;无 1例发生p16基因突变。结论　p16基因失活可能参与脑胶质瘤的发生、恶性进展及原发性脑淋巴瘤的发生。Objective To investigate the different abnormalities of p16 g ene and their correlation with the occurrence or malignant progression of brain tumor. Methods Deletion, mutation and 5'CpG island methylation were detected in 56 brain glioma, 15 meningioma and 2 primary brain lymphoma b y the use of the method of PCR, PCR-SSCP and PCR based methylation. Res ults Homozygous deletion of p16 gene were found in 18 cases of malignan t brain glioma and 1 primary brain lymphoma, 6 cases of brain glioma and 1 pr imary brain lymphoma were found to be methylated in 5'CpG island of p16 gene, wh ile mutatation of p16 gene was not found in any of the detected tumors.C onclusion Inactivation of p16 gene may be involved in the occurrence o r m alignant progression of brain glioma and genesis of primary brain lymphoma. Homo zygous deletion of p16 gene is the major mechananism for inactivation of p16 gen e

关 键 词：脑肿瘤 p16 PCR PCR-SSCP 基因缺失 CPG岛甲基化 基因突变 

分 类 号：R739.410.2[医药卫生—肿瘤]