Tsukamoto N, Morita K, Karasawa M, Omine M
Third Department of Internal Medicine, Gunma University School of Medicine, Japan.
Exp Hematol. 1992 Oct;20(9):1061-4.
DNA methylation plays an important role in gene regulation. We have analyzed the methylation status of CCGG sites in and around the human proto-oncogene c-myc in blood cells from patients with acute and chronic leukemias and with myelodysplastic syndromes using restriction endonucleases. The 5' region of c-myc was unequivocally hypomethylated in all the 58 specimens studied, including 10 from normal bone marrow and 1 from human placenta. In contrast, the 3' region was hypermethylated in a great majority of cases. However, this region was hypomethylated in 1 of 12 patients with de novo acute myeloid leukemia, 1 of 6 patients with chronic myeloid leukemia, and 4 of 5 patients with acute myeloid leukemia preceded by a documented stage of myelodysplastic syndromes. One possible mechanism for the 3' region of c-myc to have remained hypomethylated may be a "delayed methylation" during transforming events toward a more aggressive stage of the disease, but the precise mechanism is unknown.
DNA甲基化在基因调控中起重要作用。我们使用限制性内切酶分析了急性和慢性白血病以及骨髓增生异常综合征患者血细胞中人原癌基因c-myc及其周围CCGG位点的甲基化状态。在所研究的58个样本中，包括10个来自正常骨髓的样本和1个来自人胎盘的样本，c-myc的5'区域均明显低甲基化。相比之下，3'区域在大多数情况下是高甲基化的。然而，在12例新发急性髓细胞白血病患者中有1例、6例慢性髓细胞白血病患者中有1例以及5例有记录的骨髓增生异常综合征阶段后发生急性髓细胞白血病的患者中有4例，该区域是低甲基化的。c-myc的3'区域保持低甲基化的一种可能机制可能是在疾病向更具侵袭性阶段转变的过程中发生了“延迟甲基化”，但确切机制尚不清楚。
