摘要
目的 :探讨垂体腺瘤p16基因表达缺失的原因。方法 ;对无p16基因纯合性缺失的肿瘤标本进行甲基化分析。结果 :30例标本甲基化敏感性内切酶SmaI消化后p16基因第一外显子扩增片段消失 ,表明存在p16启动子的甲基化。结论
Objective:To investigate the mechanism of p16 protein expression defect in pituitary adenomas.Methods:Methylation assay was used to analyze the methylation status of p16 gene promotor in the pituitary adenomas without homozygous deletion.Results:Digested DNA from 30 cases without homozygous deletion of p16 showed no the 340bp band of exon I of p16.It indicated the methylation of p16 exonI.Conclusion:The expression defect of p16 gene in pituitary adenomas was related to the hypermethylatio of p16 gene promotor.
出处
《河南实用神经疾病杂志》
2001年第4期6-7,共2页
Henan Journal of Practical Nervous Diseases
