Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

A novel chromosomal translocation t(3;7)(q26;q21) in myeloid leukemia resulting in overexpression of EVI1

Storlazzi, CT ; Anelli, L ; Albano, F ; Zagaria, A ; Ventura, M ; Rocchi, M ; Panagopoulos, Ioannis LU ; Pannunzio, A ; Ottaviani, E and Liso, V , et al. (2004) In Annals of Hematology 83(2). p.78-83
Abstract
The EVI1 proto-oncogene encodes a nuclear zinc finger protein that acts as a transcription repressor factor. In myeloid leukemia it is often activated by chromosomal rearrangements involving band 3q26, where the gene has been mapped. Here we report two leukemia cases [a chronic myeloid leukemia blast crisis (CML-BC) and an acute myeloid leukemia (AML) M4] showing a t(3;7)(q26;q21) translocation in a balanced and unbalanced form, respectively. Fluorescent in situ hybridization (FISH) analysis revealed that both patients showed a breakpoint on chromosome 3 inside the clone RP11-33A1 containing the EVI1 oncogene and, on chromosome 7, inside the clone RP11-322M5, partially containing the CDK6 oncogene which is a D cyclin-dependent kinase gene,... (More)
The EVI1 proto-oncogene encodes a nuclear zinc finger protein that acts as a transcription repressor factor. In myeloid leukemia it is often activated by chromosomal rearrangements involving band 3q26, where the gene has been mapped. Here we report two leukemia cases [a chronic myeloid leukemia blast crisis (CML-BC) and an acute myeloid leukemia (AML) M4] showing a t(3;7)(q26;q21) translocation in a balanced and unbalanced form, respectively. Fluorescent in situ hybridization (FISH) analysis revealed that both patients showed a breakpoint on chromosome 3 inside the clone RP11-33A1 containing the EVI1 oncogene and, on chromosome 7, inside the clone RP11-322M5, partially containing the CDK6 oncogene which is a D cyclin-dependent kinase gene, observed to be overexpressed and disrupted in many hematological malignancies. Reverse transcriptase polymerase chain reaction (RT-PCR) analysis showed overexpression of EVI1 in both cases, but excluded the presence of any CDK6/EVI1 fusion transcript. CDK6 expression was also detected. Together, these data indicate that EVI1 activation is likely due not to the generation of a novel fusion gene with CDK6 but to a position effect dysregulating its transcriptional pattern. (Less)
Please use this url to cite or link to this publication:
author
; ; ; ; ; ; ; ; and , et al. (More)
; ; ; ; ; ; ; ; ; and (Less)
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
translocation t(3, gene overexpression, myeloid leukemia, EVI1, 7)
in
Annals of Hematology
volume
83
issue
2
pages
78 - 83
publisher
Springer
external identifiers
  • pmid:14551738
  • wos:000188112800002
  • scopus:10744227775
  • pmid:14551738
ISSN
1432-0584
DOI
10.1007/s00277-003-0778-y
language
English
LU publication?
yes
id
75af8e83-7bbb-4396-b3ab-024588fde18c (old id 289921)
date added to LUP
2016-04-01 12:35:34
date last changed
2022-01-27 07:11:51
@article{75af8e83-7bbb-4396-b3ab-024588fde18c,
  abstract     = {{The EVI1 proto-oncogene encodes a nuclear zinc finger protein that acts as a transcription repressor factor. In myeloid leukemia it is often activated by chromosomal rearrangements involving band 3q26, where the gene has been mapped. Here we report two leukemia cases [a chronic myeloid leukemia blast crisis (CML-BC) and an acute myeloid leukemia (AML) M4] showing a t(3;7)(q26;q21) translocation in a balanced and unbalanced form, respectively. Fluorescent in situ hybridization (FISH) analysis revealed that both patients showed a breakpoint on chromosome 3 inside the clone RP11-33A1 containing the EVI1 oncogene and, on chromosome 7, inside the clone RP11-322M5, partially containing the CDK6 oncogene which is a D cyclin-dependent kinase gene, observed to be overexpressed and disrupted in many hematological malignancies. Reverse transcriptase polymerase chain reaction (RT-PCR) analysis showed overexpression of EVI1 in both cases, but excluded the presence of any CDK6/EVI1 fusion transcript. CDK6 expression was also detected. Together, these data indicate that EVI1 activation is likely due not to the generation of a novel fusion gene with CDK6 but to a position effect dysregulating its transcriptional pattern.}},
  author       = {{Storlazzi, CT and Anelli, L and Albano, F and Zagaria, A and Ventura, M and Rocchi, M and Panagopoulos, Ioannis and Pannunzio, A and Ottaviani, E and Liso, V and Specchia, G}},
  issn         = {{1432-0584}},
  keywords     = {{translocation t(3; gene overexpression; myeloid leukemia; EVI1; 7)}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{78--83}},
  publisher    = {{Springer}},
  series       = {{Annals of Hematology}},
  title        = {{A novel chromosomal translocation t(3;7)(q26;q21) in myeloid leukemia resulting in overexpression of EVI1}},
  url          = {{http://dx.doi.org/10.1007/s00277-003-0778-y}},
  doi          = {{10.1007/s00277-003-0778-y}},
  volume       = {{83}},
  year         = {{2004}},
}