Epigenetic regulation of signal transducer and activator of transcription 3 in acute myeloid leukemia

被引：19

作者：

Ghoshal Gupta, Ampa ^{[1
]}

Baumann, Heinz ^{[2
]}

Wetzler, Meir ^{[1
]}

机构：

[1] Roswell Pk Canc Inst, Dept Med, Buffalo, NY 14263 USA

[2] Roswell Pk Canc Inst, Dept Mol & Cellular Biol, Buffalo, NY 14263 USA

来源：

LEUKEMIA RESEARCH | 2008年 / 32卷 / 07期

关键词：

signal transducer and activator of transcription 3; hypermethylation; acute myeloid leukemia;

D O I：

10.1016/j.leukres.2007.11.035

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

We have demonstrated that constitutive signal transducer and activator of transcription (STAT) 3 activity, observed in approximately 50% of acute myeloid leukemia (AML) cases, is associated with adverse treatment outcome. Constitutive STAT3 activation may result from the expression of oncogenic protein tyrosine kinases or from autocrine stimulation by hematopoietic growth factors. These causes are generally neither necessary nor sufficient for leukemogenesis; additional transforming events or growth stimulatory processes are needed. Here we review the literature addressing epigenetic regulation as a mechanism controlling STAT3 signaling in AML. A better understanding of mechanisms of dysregulation of STAT signaling pathways may serve as a basis for designing novel therapeutic strategies that target these pathways in leukemia cells. (c) 2007 Elsevier Ltd. All rights reserved.

引用

页码：1005 / 1014

页数：10

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