【摘要】 目的 :从分子水平上探索胶质瘤的发生机理。方法 :应用复合 PCR法 ,单链构象多态性 ( SSCP)分析及免疫组化的标记抗生蛋白连菌素法 ( L SAB)对脑胶质瘤 p16基因第 3外显子的纯合缺失 ,点突变以及 p16基因的表达进行了检测。结果 :2 7例胶质瘤中发现 14例有 p16基因不同程度的表达 ,但未发现纯合缺失点突变。结论 :胶质瘤中未发现 p16基因第 3外显子的纯合缺失和点突变 ,说明其在胶质瘤的发病中不是主要因素。胶质瘤中存在 p16基因的表达缺失 ,并且其表达的缺失与胶质瘤的恶性程度相关更多还原

【Abstract】 Objective: Glioma is the most common intracranial tumor but the molecular mechanism of its tumorigenesis is not clear. By using molecular biology methods we explored the molecular alterations of p16 gene of the primary glial tumors. Methods: By using multiple PCR,SSCP and LSAB we detected homozygous deletion, the mutation of exon 3 of p16 and expression of p16 gene. Results: No case of 27 gliomas was found with homozygous deletion.and the mutation of p16 gene exon 3. Expression of p16 gene was detected with different amount in 14 of 27 glioma samples. Conclusion: Homozygous deletion and the mutation of exon 3 of p16 may not be a major factor of tumorigenesis of glioma. Non expression of p16 gene in the primary glioma is correlative with the malignancy of glioma.更多还原