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 Objective: To explore the pathogenesis of glioma at the molecular level. Methods: The homozygous deletion of exon 3 of p16 gene in gliomas was detected by multiplex PCR, single strand conformation polymorphism (SSCP) analysis and immunohistochemical labeled antibiotic streptozotocin (L SAB) Point mutation and p16 gene expression were detected. Results: Fourteen of 27 gliomas showed different expression of p16 gene, but no homozygous deletion mutation was found. Conclusion: No homozygous deletions and point mutations of exon 3 of p16 gene were found in gliomas, indicating that it is not the main factor in the pathogenesis of glioma. There is a loss of expression of p16 gene in gliomas, and the lack of expression correlates with the malignancy of glioma