Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/70578
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: The granulocyte-associated transcription factor Krüppel-like factor 5 is silenced by hypermethylation in acute myeloid leukemia
Other Titles: The granulocyte-associated transcription factor Kruppel-like factor 5 is silenced by hypermethylation in acute myeloid leukemia
Author: Diakiw, S.
Kok, C.
To, L.
Lewis, I.
Brown, A.
D'Andrea, R.
Citation: Leukemia Research, 2012; 36(1):110-116
Publisher: Pergamon-Elsevier Science Ltd
Issue Date: 2012
ISSN: 0145-2126
1873-5835
Statement of
Responsibility: 
Sonya M. Diakiw, Chung H. Kok, L. Bik To, Ian D. Lewis, Anna L. Brown, Richard J. D’Andrea
Abstract: Krüppel-like factor 5 (KLF5) has been implicated as a tumor suppressor in various solid tumors such as breast and prostate, and recent studies have demonstrated a role for this protein in neutrophil differentiation of acute promyelocytic leukemia cells in response to ATRA. Here, we show that KLF5 expression increases during primary granulocyte differentiation and that expression of KLF5 is a requirement for granulocyte differentiation of 32D cells. In AML, we show that KLF5 mRNA expression levels are reduced in multiple French-American-British subtypes compared to normal controls, and also in leukemic stem cells relative to normal hematopoietic stem cells. We demonstrate that in selected AML cases, reduced expression is associated with hypermethylation of the KLF5 locus in the proximal promoter and/or intron 1, suggesting that this may represent a Class II genetic lesion in the development of AML.
Keywords: Krüppel-like factors; KLF5; Transcription factor; Granulocyte differentiation; Acute myeloid leukemia; Hypermethylation; Tumor suppressor
Rights: © 2011 Elsevier Ltd. All rights reserved.
RMID: 0020115900
DOI: 10.1016/j.leukres.2011.09.013
Appears in Collections:Molecular and Biomedical Science publications

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.