骨髓增生异常综合征和急性髓系白血病中p21（CIP 1）、p27（KIP 1）和p57（KIP 2）甲基化缺失
Absence of p21(CIP 1), p27(KIP 1) and p 57(KIP 2) methylation in MDS and AML.
作者信息
Brakensiek Kai, Länger Florian, Kreipe Hans, Lehmann Ulrich
机构信息
Institute of Pathology, Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany.
出版信息
Leuk Res. 2005 Nov;29(11):1357-60. doi: 10.1016/j.leukres.2005.04.012.
Transcriptional silencing of tumour suppressor genes (TSG) due to hypermethylation is a common event in human tumours. The three members of the KIP/CIP family of cyclin dependent kinase inhibitors (CDKIs), p21(CIP 1), p27(KIP 1), and p 57(KIP 2), play key roles in cell cycle regulation, but little is known about their methylation in myeloid neoplasia. Therefore, we analysed 9 haematopoietic cell lines, 67 myelodysplastic syndrome (MDS) and 26 acute myeloid leukaemia (AML) cases as well as 11 controls. p 57(KIP 2) hypermethylation was found in 4/9 cell lines, but methylation of p21(CIP 1) and p27(KIP 1) was infrequent. All patient samples analysed were methylation-negative for these three genes.
由于高甲基化导致的肿瘤抑制基因（TSG）转录沉默在人类肿瘤中是常见现象。细胞周期蛋白依赖性激酶抑制剂（CDKIs）的KIP/CIP家族的三个成员，即p21（CIP 1）、p27（KIP 1）和p57（KIP 2），在细胞周期调控中起关键作用，但关于它们在髓系肿瘤中的甲基化情况知之甚少。因此，我们分析了9个造血细胞系、67例骨髓增生异常综合征（MDS）和26例急性髓系白血病（AML）病例以及11例对照。在4/9的细胞系中发现了p57（KIP 2）高甲基化，但p21（CIP 1）和p27（KIP 1）的甲基化并不常见。所有分析的患者样本这三个基因的甲基化均为阴性。
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