脑胶质瘤抑瘤基因p53、p16缺失、变异与肿瘤恶性程度的相关性

目的：探索肿瘤抑制基因ｐ５３、ｐ１６缺失、变异与肿瘤恶性程度的关系。方法：对３１例脑胶质瘤的原发肿瘤标本行ｐ５３、ｐ１６蛋白检测，用免疫组化ＬＳＡＢ法。结果：星形细胞瘤Ⅰ级１７例中，ｐ１６１０例表达３０％以下，７例不表达，ｐ５３４例表达３０％以下，１３例不表达；星形细胞瘤Ⅱ级９例中，ｐ１６１例表达３０％以下，８例不表达，ｐ５３３例表达３０％以下，１例表达３０％～６０％，５例不表达；星形细胞瘤Ⅲ级２例，ｐ１６均不表达，ｐ５３１例表达３０％以下，１例表达３０％～６０％；星形细胞瘤Ⅳ级３例，ｐ１６均不表达，ｐ５３表达均在３０％～６０％。结论：ｐ５３失活主要见于恶性胶质瘤和恶性发展中的胶质瘤，肿瘤的恶性程度越高，ｐ５３蛋白失活越严重。偏良性的胶质瘤ｐ５３呈轻度阳性表达时，提示肿瘤可能处于早期恶性变过程中。ｐ１６缺失主要见于星形细胞瘤Ⅱ、Ⅲ、Ⅳ级等恶性胶质瘤。

A study of relation between human glioma malignanty and its p53 p16 protein lackage and mutation

Objective: To investigate the relation between p53 and p16 tumor suppresor gene mutation and lackage and glioma malignanty.Methods: p53 and p16 protein within 31 cases primary human brain glioma were inmmuno histochemistrically studied.Results: Within 17 cases Ⅰ grading astrocytoma,10 cases p16 expressed under 30% while 7 no expresion.4 cases p53 expressed over 30% with 13 none.Within 9 cases Ⅱ grading astrocytoma,one p16 expressed under 30%,8 had no expression.3 cases p53 expressed under 30%,one expressed from 30% to 60%,5 cases had no expresion.As for 2 cases Ⅲ grading astrocytoma,p16 had all no expresion with one p53 expressed under 30% and another one expressed from 30% to 60%.Within 3 cases glioblastoma no p16 expressed while p53 expressed from 30% to 60%.Conclusion: p53 mutation were mainly seen in the malignant and the malignant transforming glioma,the high malignant ones have more p53 mutation.When p53 lowerly expressed in the less malignant tumor,it suggest that the tumor be undertaking malignant transformation.p16 lackage were mainly seen within Ⅱ Ⅲ grading astrocytoma and glioblastoma.