Journal
FEBS LETTERS
Volume 584, Issue 12, Pages 2662-2669Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2010.04.002
Keywords
Acute myeloid leukemia; Oncofusion protein; Transcriptional regulation; Epigenetic
Funding
- European Union [LSHC-CT-2005-518417]
- Dutch Cancer Foundation [KWF KUN 2009-4527]
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Acute myeloid leukemia (AML) associated translocations often cause gene fusions that encode onco-fusion proteins. Although many of the breakpoints involved in chromosomal translocations have been cloned, in most cases the role of the chimeric proteins in tumorigenesis is not elucidated. Here we will discuss the fusion proteins of the 4 most common translocations associated with AML as well as the common molecular mechanisms that these four and other fusion proteins utilize to transform progenitor cells. Intriguingly, although the individual partners within the fusion proteins represent a wide variety of cellular functions, at the molecular level many commodities can be found. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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