摘要
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 。
Objective: Glioma is the most common intracranial tumor but the molecular mechanism of its tumorigenesis is not clear. By using molecular biologic methods we explored the molecular alterations of chromosome 3p24 of the primary glial tumors. Methods: We performed restriction fragment length polymorphism (RFLP) analysis by using the polymerase chain reaction (PCR) and primer sets of two DNA markers to examine loss of heterozygosity (LOH) from 3p in glioma samples. Results: Among six informative cases at EA β H loci, three exhibited LOH, but we could not find LOH at EA β MD loci. Conclusion: LOH at EA β H loci of 3p24 was found in the gradeⅡ and gradeⅣ gliomas. So we thought that the gene with LOH may play some role in tumorigenesis and malignancy of glial tumors.
出处
《新疆医科大学学报》
CAS
2000年第3期216-218,共3页
Journal of Xinjiang Medical University
