DEK oncogene expression during normal hematopoiesis and in Acute Myeloid Leukemia (AML)

Gemma E. Logan, Nirit Mor-Vaknin, Till Braunschweig, Edgar Jost, Pia Verena Schmidt, David M. Markovitz, Ken I. Mills, Ferdinand Kappes, Melanie J. Percy

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)
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Abstract

DEK is important in regulating cellular processes including proliferation, differentiation and maintenance of stem cell phenotype. The translocation t(6;9) in Acute Myeloid Leukemia (AML), which fuses DEK with NUP214, confers a poor prognosis and a higher risk of relapse. The over-expression of DEK in AML has been reported, but different studies have shown diminished levels in pediatric and promyelocytic leukemias. This study has characterized DEK expression, in silico, using a large multi-center cohort of leukemic and normal control cases. Overall, DEK was under-expressed in AML compared to normal bone marrow (NBM). Studying specific subtypes of AML confirmed either no significant change or a significant reduction in DEK expression compared to NBM. Importantly, the similarity of DEK expression between AML and NBM was confirmed using immunohistochemistry analysis of tissue mircorarrays. In addition, stratification of AML patients based on median DEK expression levels indicated that DEK showed no effect on the overall survival of patients. DEK expression during normal hematopoiesis did reveal a relationship with specific cell types implicating a distinct function during myeloid differentiation. Whilst DEK may play a potential role in hematopoiesis, it remains to be established whether it is important for leukemagenesis, except when involved in the t(6;9) translocation.
Original languageEnglish
Pages (from-to)123-131
Number of pages9
JournalBlood Cells, Molecules and Diseases
Volume54
Issue number1
Early online date12 Aug 2014
DOIs
Publication statusPublished - Jan 2015

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