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通过DNMT3A调解的CpG岛超甲基化是AML进展的结果

David H Spencer¹, David A Russler-Germain², Shamika Ketkar²

¹Section of Stem Cell Biology, Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; The McDonnell Genome Institute, Washington University, St. Louis, MO 63110, USA.

|February 21, 2017

概括

在急性髓性白血病 (AML) 中,DNMT3A突变与DNA低甲基化有关,这可能会引发疾病. CpG岛的甲基化似乎是AML进展的结果,而不是原因.

科学领域:

基因组学
表观遗传学
癌症生物学

背景情况:

大约25%的急性髓性白血病 (AML) 患者发现了DNMT3A突变.
常见的DNMT3A^R882H突变表现出主导负活性,在体外显著降低了DNA甲基化.

研究的目的:

研究DNMT3A依赖DNA甲基化在白血病发生中的作用.
区分低甲基化和高甲基化在AML发展中的作用.

主要方法:

在具有或没有DNMT3A^R882突变的AML患者的原发性白血病和非白血病细胞上进行了全基因组双硫酸序列测定.
与DNMT3A突变状态和细胞增殖相关的DNA甲基化模式的分析.

主要成果:

具有DNMT3A^R882H突变的非白血病造血细胞显示焦点DNA低甲基化,这表明它在AML之前.
野生型DNMT3A的AML表现出CpG岛屿过甲基化,但在DNMT3A^R882突变AML中没有这种情况,并且与基因沉默无关.
初级造血干细胞在细胞因子扩张时显示DNMT3A依赖的高甲基化,这表明它可能是对增殖的反应.

结论:

由DNMT3A^R882突变驱动的低甲基化是AML发病的早期事件.
依赖DNMT3A的CpG岛的高甲基化是AML进展的下游后果,而不是起始因素.

关键词:

洗钱问题 CpG 岛屿过甲基化 DNA 甲基化在 DNMT3A 癌症

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