目的 :从分子水平上探索胶质瘤的发生机理 ,为胶质瘤的诊断、预后提供有意义的指标 ,并且为基因治疗胶质瘤提供理论依据。方法 :应用 PCR技术配合限制性片段长度多态性 (RFL P)分析 ,对胶质瘤 3号染色体短臂3p2 4两个 DNA标志不同位点的杂合缺失 (L OH)进行检测。结果 :2 7例胶质瘤标本中在 EAβH位点发现 6个信息个体中有 3例显示杂合缺失 ,杂合缺失率为 3/ 6 ,而 EAβ MD位点未发现杂合缺失。 结论 :胶质瘤中未发现 3p2 4EAβ MD等位基因的杂合缺失 ,说明该基因可能不参与胶质瘤的发生发展过程 ;3p2 4EAβ H等位基因的杂合缺失存在于 级和 级胶质瘤中 ,说明该基因可能在胶质瘤的发生发展过程中起一定作用 Objective: To explore the mechanism of glioma at the molecular level, to provide a meaningful indicator for the diagnosis and prognosis of gliomas, and to provide a theoretical basis for gene therapy of glioma. Methods: PCR-based restriction fragment length polymorphism (RFLP) analysis was used to detect the heterozygous deletion (LOH) at different DNA markers of 3p24 in the short arm of chromosome 3 of glioma. RESULTS: Three of the 6 informative individuals found heterozygous deletions in 3 of 6 individuals at the site of EAβH in 27 samples of gliomas, showing a loss of heterozygosity of 3/6, but no heterozygous deletions were found at the site of EAβ MD. Conclusion: The heterozygous deletion of 3p2 4EAβ MD allele was not found in gliomas, indicating that this gene may not participate in the development and progression of gliomas. The heterozygous deletion of 3p2 4EAβ H allele exists in both glomerulus Tumor, indicating that the gene may play a role in the development of glioma