期刊
BLOOD CELLS MOLECULES AND DISEASES
卷 53, 期 1-2, 页码 67-76出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bcmd.2014.01.002
关键词
Leukemogenesis; Oncogenes; EVI1; Myeloid leukemia; Apoptosis; Differentiation
类别
资金
- National Institutes of Health (NIH) [R01CAl20313]
- New York State Stem Cell Science (NYSTEM) [CO26423]
- Alex's Lemonade Stand Foundation (ALSF)
- Children's Leukemia Research Association (CLRA)
- National Heart Lung Blood Institute - University of Rochester Clinical Translational Research Institute
The EVI1 oncogene at human chr 3q26 is rearranged and/or overexpressed in a subset of acute myeloid leukemias and myelodysplasias. The EVI1 protein is a 135 kDa transcriptional regulator with DNA-binding zinc finger domains. Here we provide a critical review of the current state of research into the molecular mechanisms by which this gene plays a role in myeloid malignancies. The major pertinent cellular effects are blocking myeloid differentiation and preventing cellular apoptosis, and several potential mechanisms for these phenomena have been identified. Evidence supports a role for EVI1 in inducing cellular quiescence, and this may contribute to the resistance to chemotherapy seen in patients with neoplasms that overexpress EVI1 Another isoform, MDS1EVI1 (or PRDM3), encoded by the same locus as EVI1, harbors an N-terminal histone methyltransferase(HMT) domain; experimental findings indicate that this protein and its HMT activity are critical for the progression of a subset of AMLs, and this provides a potential target for therapeutic intervention. (C) 2014 Published by Elsevier Inc.
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