原发与复发性成胶质细胞瘤中DNA错配修复蛋白、p53蛋白表达和DNA倍性的差异  

Differences of Expression of DNA Mismatch Repair,p53Proteins ,and DNA Ploidy between Primary and Secondary Glioblastomas

作　　者：谢丹[1] 王海军[2] 文剑明[1] 陶瑜[1] 张萌[1] 陈明振[2] 钟思陶[1] 

机构地区：[1]中山医科大学病理学教研室,广东广州510089 [2]中山医科大学附属第一医院神经外科,广东广州510080

出　　处：《癌症》2001年第10期1038-1042,共5页Chinese Journal of Cancer

基　　金：香港"中华人民共和国学者MrsIvyWu研究基金"项目(1999~2000.NO7)

摘　　要：目的:探讨原发与复发性成胶质细胞瘤的临床病理特点和分子遗传学差异。方法:应用免疫组化和流式细胞学方法对32例广东籍成胶质细胞瘤hMSH2,hMLH1和p53蛋白表达及DNA倍性进行检测,结合临床病理学资料,分析它们之间的相关性。结果:32例成胶质细胞瘤患者的DNA倍性与p53的表达存在显著的相关性P0.05,23例非整倍体DNA含量的肿瘤中,有20例87.0%出现p53蛋白的过度表达。在原发与复发性成胶质细胞瘤中,肿瘤的DNA含量和p53蛋白表达有显著的差异性P<0.05,复发性成胶质细胞瘤中,有87.5%14/16出现了p53蛋白的过度表达,93.8%15/16为非整倍体的DNA含量;而原发性成胶质细胞瘤,则有56.3%9/16呈p53表达正常表达,50.0%8/16是二倍体或近二倍体DNA含量。另外,丢失了hMSH2蛋白的2例成胶质细胞瘤,全部是复发性的肿瘤,均呈p53蛋白的过度表达和非整倍体的DNA含量。结论:广东籍成胶质细胞瘤患者的发病年龄明显低于欧美人。绝大多数的复发性成胶质细胞瘤是沿染色体不稳定性Chromosomalinstability,CI途径而发展,多数出现p53基因的异常表达,少部分肿瘤可同时涉及微卫星不稳定Microsatellite.instability,MSI途径;约一半的原发性成胶质细胞瘤既不沿CI途径发展,也未出现p53基因的异常,同时又无证据显示与MSI途径有关。Objective：To investigate the clinicopatholog ic ch aracters and molecular genetic differences between primary and secondary gliobla stoma s in Guangdong．Methods ：Immunohistochemistry and Flow cyto metry methods were used to detect the expression of hMSH ２ ，hMLH １ ，p５３proteins and status of DNA ploidy in ３２cases of glioblastomas in Gu angdong，and analyze their correlations with the patient's cancergenetic pathway s．Results：The mean age of ３２glioblastomas in Guangdong was ３３．５years old ．There was a significant correlation between DN A ploidy and expression of p５ ３protein in this glioblastoma group（P＜０．０５）．Of the ２３ glioblastomas had aneuploid DNA con tent，２０cases（８７．０％）sh owed overexpression of p５３．There were significant differences of DNA ploidy and p５３exp ression between primary and secondary glioblastomas（P＜０．０５） ．Of the １６secondary glioblastomas，fourteen（１４／１６）showed overexpressio n of p５３protein and fifteen（１５／１６）had aneuploid DNA content，while with in the １６prim ary glioblastomas，nine（９／１６）cases were detected with norm al expr ession of p５３protein，eight （８／１６）showed DNA diploid or near－di ploid．In addition，there existed two （２／３２）cases of secondary glioblastom as with the loss of hMSH２protein had overexpression of p５３an d aneuploid DNA content．Conclusions ：Most secondary glioblastomas is via Chro mosomal instabil ity（CI ）pathway，the majority of them showed aberration of p５３gene，and few of them also involved in Micro satellite instability（MSI ）pathway．About half of primary gliob lastomas with the nor－mal expression of p５３gene showed no e vidence of either CI or MSI cancergen etic pathway．

关 键 词：成胶质细胞瘤 错配修复基因 免疫组织化学 流式细胞术 DNA P53蛋白 

分 类 号：R730.2[医药卫生—肿瘤]