Cui Wen, Wu Renliang, Cao Huiling, Gao Jifa, Wang Xu, Ren Qiwei
Department of Pathology, Short of Basic Medical Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
J Huazhong Univ Sci Technolog Med Sci. 2005;25(6):622-4, 635. doi: 10.1007/BF02896152.
To investigate the effect of P53 protein accumulation and p53 gene mutation in the pathogenesis of glioma and to study the role of MDM2, P53 and P16 protein in glioma formation and progression and their relationship with each other, LSAB immunohistochemical staining method and non-isotopic PCR-SSCP techniques were used to detect the expression of MDM2, P53 and P16 protein and p53 gene mutation in 48 cases of gliomas. The results showed that the positive expression rate of MDM2, P53 and the negative rate of P16 was 22.9%, 41.7% and 60.4%, respectively. The latter two in high grade (grade III, IV) gliomas had a significantly higher rate than in the low grade (grade II) gliomas. Moreover, the co-expression of MDM2 and P53 protein was confirmed in only 1 of 48 cases. No significant difference was found in the rate of the expression of MDM2 between high grade and low grade gliomas (P > 0.1). PCR-SSCP results showed that mutation of 5-8 exons of p53 gene was detected in 17 out of 48 cases (35.42%). Mutation was detected in 16 of 20 cases of positive p53 expression, and another one was detected in 28 cases of negative expression cases. The correlation between p53 mutation and p53 immunopositivity was observed in 89.6% of the cases. P53 gene mutation and the level of MDM2, P53 and P16 protein were not related to age, gender of the patients, tumor location and size. It is concluded that the mutation of p53 and deletion of p16 might play important roles in the tumorigenesis of gliomas and it was significantly associated with the grade of tumor differentiation. P53 protein accumulation can indirectly reflect p53 mutation. MDM2 amplification and overexpression might be an early event in the growth of human gliomas.
为探讨P53蛋白积聚及p53基因突变在胶质瘤发病机制中的作用,研究MDM2、P53及P16蛋白在胶质瘤发生发展中的作用及其相互关系,采用LSAB免疫组化染色法及非同位素PCR-SSCP技术检测48例胶质瘤中MDM2、P53及P16蛋白的表达及p53基因突变情况。结果显示,MDM2阳性表达率、P53阳性表达率及P16阴性表达率分别为22.9%、41.7%及60.4%。后两者在高级别(Ⅲ、Ⅳ级)胶质瘤中的表达率显著高于低级别(Ⅱ级)胶质瘤。此外,48例中仅1例证实MDM2与P53蛋白共表达。高级别与低级别胶质瘤中MDM2表达率差异无统计学意义(P>0.1)。PCR-SSCP结果显示,48例中有17例(35.42%)检测到p53基因5~8外显子突变。p53表达阳性的20例中有16例检测到突变,p53表达阴性的28例中有1例检测到突变。89.6%的病例观察到p53突变与p53免疫阳性之间存在相关性。p53基因突变及MDM2、P53和P16蛋白水平与患者年龄、性别、肿瘤部位及大小无关。结论:p53突变及p16缺失可能在胶质瘤的发生中起重要作用,且与肿瘤分化程度显著相关。P53蛋白积聚可间接反映p53突变。MDM2扩增及过表达可能是人类胶质瘤生长过程中的早期事件。