上皮源性恶性肿瘤患者p16/MTS1抑癌基因失活研究  

Inactivation of the p16/MTS1 Gene in Multiple Human Cancers

作　　者：高居忠[1] 朱章菱[1] 肖白[1] 王跃[1] 迟闺珠[1] 于莎莎[1] 刘复兴 李正廷[1] 张愚[1] 

机构地区：[1]首都医科大学附属北京红十字朝阳医院

出　　处：《首都医科大学学报》2000年第1期33-36,共4页Journal of Capital Medical University

基　　金：北京市卫生局科学基金

摘　　要：以不同种类的上皮源性恶性肿瘤患者为研究对象 ,分析肿瘤组织中p1 6 /MTS1基因纯合缺失、异常甲基化和表达缺失。发现 p1 6基因纯合缺失率为 1 4% ( 1 5 /1 0 8) ;异常甲基化检出率为 1 4% ( 8/5 8) ;p1 6蛋白表达缺失率为4 4% ( 2 8/6 3) ;按组织学分级 ,中、低分化组 p1 6蛋白表达缺失率显著高于高分化组 (P <0 .0 5 )。p1 6基因失活患者普遍预后差。肺癌、食管癌患者 p1 6基因失活者 1 7例 ,手术后 6个月内 6例死亡 ,1例转移 ;p1 6基因发生缺失和异常甲基化的 6例膀胱癌患者中 4例复发。研究结果表明 ,p1 6基因失活在上皮源性恶性肿瘤患者中是较为常见的基因变化 ,与患者的病理分级和预后有密切关系。Inactivation of the p16/MTS1 gene was examined by homozygous deletion, methylation of 5′ CpG islands and silencing of expression in multiple tumor samples from patients. Homozygous deletion and de novo methylation of the gene were confirmed in 15(14%) of 108 and 8(14%) of 58 patients, respectively. Protein product of p16 was detected by immunohistochemical method. Rate of p16 gene expressive deletion was 44% (28/63). The p16 deletion rates were significantly higher in poorly differen tiated group. In accordance with following up the patients, 6 cases died and 1 case metastasized after operation in a half year in 17 patients with lung cancer or esophageal carcinoma whose p16 gene was inactivated; 4 cases recurred in 6 patients with bladder cancer whose p16 gene were homozygously deleted or methylated. These results suggested that inactivation of the p16 gene appeared to be a common event in multiple cancers and might be associated with histological grade and prognosis.

关 键 词：P16/MTS1 抑癌基因 失活 上皮源性肿瘤 

分 类 号：R730.45[医药卫生—肿瘤]