The role of EVI1 in myeloid malignancies.

Published

Journal Article (Review)

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, MDS1-EVI1 (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.

Full Text

Duke Authors

Cited Authors

  • Glass, C; Wilson, M; Gonzalez, R; Zhang, Y; Perkins, AS

Published Date

  • June 2014

Published In

Volume / Issue

  • 53 / 1-2

Start / End Page

  • 67 - 76

PubMed ID

  • 24495476

Pubmed Central ID

  • 24495476

Electronic International Standard Serial Number (EISSN)

  • 1096-0961

Digital Object Identifier (DOI)

  • 10.1016/j.bcmd.2014.01.002

Language

  • eng

Conference Location

  • United States