The EVI-1 gene — its role in pathogenesis of human leukemias

Abstract 

EVI-1 (ecotropic virus integration site-1) was at first identified as an integration site of the murine leukemia retrovirus in murine myeloid leukemias. It is involved in pathogenesis of mouse and human leukemias. EVI-1 expression may be activated by retroviral insertion or is caused by chromosomal translocations. EVI-1 gene is located on human chromosome 3, spans over 100 kb and contains 12 exons with ten coding exons. EVI-1 gene encodes 1051 amino acids DNA binding protein containing ten zinc finger repeats organized in two domains. The 145 kDa EVI-1 protein is localized in the nucleus. The structure of the EVI-1 protein indicates that it functions as a transcriptional factor of the zinc finger family. The role of this transcription factor in myeloid cell transformation and the target genes of EVI-1 is still unknown. Occurence of a few EVI-1 fusion transcripts was shown. The role of this fusion proteins is still unclear. Mouse and human sequences of the gene show a high degree of homology; 91% in nucleotide sequence and 94% in amino acid sequence.

Keywords:  EVI-1, 3q26, Zn finger protein, Leukemia

Abbreviations:  Abl, Abelson gene, AML, acute myeloid leukemia, BC, blast crisis, Bcr, breakpoint cluster region, CML, chronic myelocytic leukemia, D1-cons, the first consensus sequence, D2-cons, the second consensus sequence, JMML, juvenile myelomonocytic leukemia, MDS, myelodysplastis syndrome, PR, proline rich region, RT-PCR, reverse transcription and polymerase chain reaction