Absence of p21CIP1, p27KIP1 and p57KIP2 methylation in MDS and AML

被引：39

作者：

Brakensiek, K ^{[1
]}

Länger, F ^{[1
]}

Kreipe, H ^{[1
]}

Lehmann, U ^{[1
]}

机构：

[1] Hannover Med Sch, Inst Pathol, D-30625 Hannover, Germany

来源：

LEUKEMIA RESEARCH | 2005年 / 29卷 / 11期

关键词：

p21(CIP1); p27(KIP1); p57(KIP2); methylation; MDS; AML; quantitative real-time PCR;

D O I：

10.1016/j.leukres.2005.04.012

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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(CIP1), p27(KIP1), and p57(KIP2), 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. p57(KIP2) hypermethylation was found in 4/9 cell lines, but methylation of p21(CIP1) and p27(KIP1) was infrequent. All patient samples analysed were methylation-negative for these three genes. (c) 2005 Elsevier Ltd. All rights reserved.

引用

页码：1357 / 1360

页数：4

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