3q26/EVI1 rearrangements in myeloid hemopathies: a cytogenetic review

The EVI1 gene, located in chromosomal band 3q26, is a transcription factor that has stem cell-specific expression pattern and is essential for the regulation of self-renewal of hematopoietic stem cells. It is now recognized as one of the dominant oncogenes associated with myeloid leukemia. EVI1 over...

Full description

Saved in:
Bibliographic Details
Published in:Future oncology (London, England) England), 2015-06, Vol.11 (11), p.1675-1686
Main Authors: De Braekeleer, Marc, Le Bris, Marie-Josée, De Braekeleer, Etienne, Basinko, Audrey, Morel, Frédéric, Douet-Guilbert, Nathalie
Format: Article
Language:English
Subjects:
Chromosome Breakpoints
Chromosomes, Human, Pair 3
DNA-Binding Proteins - genetics
Gene Expression
Gene Rearrangement
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics
Leukemia, Myeloid, Acute - genetics
MDS1 and EVI1 Complex Locus Protein
Proto-Oncogenes - genetics
Transcription Factors - genetics
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The EVI1 gene, located in chromosomal band 3q26, is a transcription factor that has stem cell-specific expression pattern and is essential for the regulation of self-renewal of hematopoietic stem cells. It is now recognized as one of the dominant oncogenes associated with myeloid leukemia. EVI1 overexpression is associated with minimal to no response to chemotherapy and poor clinical outcome. Several chromosomal rearrangements involving band 3q26 are known to induce EVI1 overexpression. They are mainly found in acute myeloid leukemia and blastic phase of Philadelphia chromosome-positive chronic myeloid leukemia, more rarely in myelodysplastic syndromes. They include inv(3)(q21q26), t(3;3)(q21;q26), t(3;21)(q26;q22), t(3;12)(q26;p13) and t(2;3)(p15-23;q26). However, many other chromosomal rearrangements involving 3q26/EVI1 have been identified. The precise molecular event has not been elucidated in the majority of these chromosomal abnormalities and most gene partners remain unknown.
ISSN:1479-6694
1744-8301
DOI:10.2217/fon.15.64