Department of Hematology, Affiliated People's Hospital of Jiangsu University, 8 Dianli Road, Zhenjiang, 212002, China.
Leuk Res. 2010 Aug;34(8):991-4. doi: 10.1016/j.leukres.2010.01.003. Epub 2010 Jan 29.
The epigenetic changes of tumor suppressor genes are now recognized as an alternative mechanism contributing to the development of myelodysplastic syndrome (MDS). The expression of DNA-damage-inducible transcript 3 (DDIT3) gene has been found down-regulated in myeloid malignancies including MDS. In this study, we performed methylation-specific PCR (MSP) to investigate the methylation status of the CpG island of DDIT3 promoter region in MDS. Aberrant methylation of DDIT3 was detected in 31.8% (21/66) of the cases analyzed. No correlation was found between DDIT3 promoter methylation and clinical parameters and MDS subtypes. Although the estimated 50% survival time of the methylated DDIT3 group was shorter than that of unmethylated group (12.0 months vs. 23.0 months), the difference was not statistically significant (P=0.137). These findings suggest that the hypermethylation of DDIT3 promoter might be one of early events in the development of MDS.
肿瘤抑制基因的表观遗传改变现在被认为是导致骨髓增生异常综合征（MDS）的另一种机制。已经发现 DNA 损伤诱导转录物 3（DDIT3）基因在包括 MDS 在内的髓系恶性肿瘤中的表达下调。在这项研究中，我们通过甲基化特异性 PCR（MSP）来研究 MDS 中 DDIT3 启动子区域 CpG 岛的甲基化状态。分析的 66 例病例中有 31.8%（21/66）存在 DDIT3 异常甲基化。DDIT3 启动子甲基化与临床参数和 MDS 亚型之间没有相关性。虽然甲基化 DDIT3 组的估计 50%生存时间短于未甲基化组（12.0 个月比 23.0 个月），但差异无统计学意义（P=0.137）。这些发现表明 DDIT3 启动子的高甲基化可能是 MDS 发展过程中的早期事件之一。
