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出 处:《世界肿瘤杂志》2009年第3期152-157,共6页Tumour Journal of the World
摘 要:目的探讨p73基因异常甲基化在非霍奇金淋巴瘤(non—Hodgkin’s lymphomas,NHL)中的分布,去甲基化p73基因的再表达。方法采用甲基化特异性PCR(Methylation specific polymerase chain reaction,MSP)方法检测22例非霍奇金淋巴瘤p73基因CpG岛甲基化状态。使用反转录PCR(Reverse transoription polymerase chain reaction,RT-PCR)方法检测CdR药物作用前后P73基因mRNA的表达情况。结果非霍奇金淋巴瘤p73基因甲基化的发生率为27.3%(6/22),高度恶性比低度恶性更易发生甲基化,其发生率分别为42.8%和0%,5-杂氮-2’.脱氧胞嘧啶(5-aza-2’-deoxycytidine,CdR)在4.0~8.0μmol/L时可诱导非霍奇金淋巴瘤细胞p73去甲基化。结论p73基因甲基化可能是非霍奇金淋巴瘤发病的原因之一,去甲基化治疗是可行的。Objectives To illustrate the expression of p73 gene methylation and how to recover p73 gene expression and produce antitumor effect by demethylation in NHL. Methods MSP is used to determine whether p73 gene is methylation or not. we use RT-PCR to detect p73 gene expression before and after being treated with CdR. Results The results have showed that 27.75% (6/22) in NHL is methylation in p73 gene, and methylation was much more frequently in high grade NHLs (42.8%) than in low grade NHLs (0%). p73 gene can be demethylated and reexpressed with CdR of 4.0-8.0μmol/L concentration. Conclusions The hypemethylation of p73 gene may be me of the reason of oncogenesis in NHL and the method of p73 gene of demethylation provides an experimental foundation for hematologic malignant clinical therapy.
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