Comparison of promoter DNA methylation and expression levels of genes encoding CCAAT/enhancer binding proteins in AML patients

被引:21
作者
Musialik, Ewa [1 ]
Bujko, Mateusz [1 ]
Kober, Paulina [1 ]
Grygorowicz, Monika Anna [2 ]
Libura, Marta [3 ]
Przestrzelska, Marta [3 ]
Juszczynski, Przemyslaw [4 ]
Borg, Katarzyna [4 ]
Florek, Izabela [5 ]
Jakobczyk, Malgorzata [5 ]
Baranowska, Alicja [6 ]
Siedlecki, Janusz Aleksander [1 ]
机构
[1] Maria Sklodowska Curie Mem Canc Ctr & Inst Oncol, Dept Mol & Translat Oncol, PL-02781 Warsaw, Poland
[2] Maria Sklodowska Curie Mem Canc Ctr & Inst Oncol, Dept Immunol, PL-02781 Warsaw, Poland
[3] Med Univ Warsaw, Dept Hematol Oncol & Internal Dis, Warsaw, Poland
[4] Inst Hematol & Transfus Med, Dept Diagnost Hematol, Warsaw, Poland
[5] Jagiellonian Univ, Dept Hematol, Krakow, Poland
[6] Marian Weiss Mem Mazowia Rehabil Ctr, Neuroortoped Dept, Konstancin Jeziorna, Poland
关键词
Acute myelogenous leukemia; CCAAT/enhancer binding protein; CEBPA; CEBPD; CEBPE; CEBPZ(DDIT3); DNA methylation; Gene expression; ACUTE MYELOID-LEUKEMIA; FACTOR-C/EBP-ALPHA; TRANSCRIPTION FACTOR; EUROPEAN LEUKEMIANET; CEBPA; HYPERMETHYLATION; DIFFERENTIATION; MUTATIONS; CYTOGENETICS; ADULTS;
D O I
10.1016/j.leukres.2014.04.013
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
CCAAT/enhancer binding proteins (CEBPs) are transcription factors regulating myeloid differentiation. Disturbances of their expression may contribute to leukemogenesis. In this study we compared promoter methylation and expression levels of selected CEBP genes in a group of 78 AML patients, normal bone marrow and hematopoietic precursor cells. CEBPA, CEBPD and CEBPE promoter methylation levels were elevated in 37%, 35.5% and 56.7% of patients. No CEBPZ(DDIT3) methylation was observed. An inverse relationship between CEBPA and CEBPD DNA methylation and expression levels was observed. AML cytogenetic risk groups and patients with particular translocation are characterized by distinct methylation/expression profile of CEBPs encoding genes. (C) 2014 Elsevier Ltd. All rights reserved.
引用
收藏
页码:850 / 856
页数:7
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