γ射线诱发小鼠白血病模型中p16基因的改变

目的：研究γ射线诱发小鼠白血病模型中p16基因的失活机制。方法：应用聚合酶链反应(PcR)扩增39例γ射线诱发的白血病和对照小鼠胸腺组织中p16基因第1、第2外显子，检测等位基因纯合性缺失；用限制性内切酶-PCR法检测p16基因的甲基化发生情况；并应用PCR-单链构象多态性分析银染方法检测p16基因碱基突变的发生。结果：在白血病模型中，外显子2的缺失率为33．3％，甲基化的发生率为23．1％。结论：γ射线诱发的小鼠白血病模型发生、发展过程中伴有p16基因的改变，其失活以纯合性缺失和甲基化为主。

Alterations of p16 gene in mice leukemia model induced by γ-ray irradiat ion

Objective: To investigate the mechanism of p16 gene inactivation in the mice leukemia model induced by γ-ray irradiation.M ethods: PCR technique was used to amplify exon 1 and 2 of p16 gene and to detect the homozygous deletion.The occurrence of methylation in the 5′CpG island was studied with restriction enzyme-PCR.PCR-SSCP-silver staining technique was used to detect mutation of p16 gene.Results: The deletion rate of the exon 2 and the methylatio n of CpG island in mice leukemia model were 33.3% and 23.1% respectively.Conclusion: The alteration of p16 gene is involved in the de velopment of the mice leukemia induced by γ-ray irradiation.The homozygous del etion and methylation are the main manners accounting for inactivation of p16 gene in mice.