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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)
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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 Verlag
external identifiers
  • pmid:14551738
  • wos:000188112800002
  • scopus:10744227775
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
2007-11-02 09:48:10
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2017-10-22 03:56:52
@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},
  keyword      = {translocation t(3,gene overexpression,myeloid leukemia,EVI1,7)},
  language     = {eng},
  number       = {2},
  pages        = {78--83},
  publisher    = {Springer Verlag},
  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},
  volume       = {83},
  year         = {2004},
}