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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 clinicopathological features and molecular genetic differences of primary and recurrent glioblastomas. Methods: Immunohistochemistry and flow cytometry were used to detect the expression of hMSH2, hMLH1 and p53 protein and DNA ploidy in 32 cases of glioblastoma from Guangdong. The correlation between them was analyzed by combining with clinical pathology data. RESULTS: There was a significant correlation between DNA ploidy and p53 expression in 32 glioblastoma patients. Among the tumors with aneuploid DNA content in 23 cases, overexpression of p53 protein was found in 87 of 20 tumors with aneuploid DNA content. . In primary and recurrent glioblastomas, the DNA content of tumors and p53 protein expression were significantly different (P<0.05). Among recurrent glioblastomas, 87.5% of 14/16 showed p53 protein. Overexpressed, 93.8% of 15/16 was aneuploid DNA content; whereas in primary glioblastoma, 56.3% of 9/16 showed normal expression of p53, and 50.0% of 8/16 was diploid or Near diploid DNA content. In addition, two cases of glioblastoma with loss of hMSH2 protein, all of which were recurrent tumors, all showed p53 protein overexpression and aneuploid DNA content. Conclusion: The incidence age of glioblastoma patients in Guangdong is significantly lower than that of European and American people. The vast majority of recurrent glioblastomas develop along Chromosomalinstability (CI) pathway, most of which show abnormal expression of p53 gene, and a few tumors can simultaneously involve microsatellite.instability, MSI pathway; Half of the primary glioblastomas did not develop along the CI pathway, nor did they show abnormalities in the p53 gene, and there was no evidence that the MSI pathway was involved.