A novel chromosomal translocation t(3;7)(q26;q21) in myeloid leukemia resulting in overexpression of EVI1
(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:
https://lup.lub.lu.se/record/289921
- author
- organization
- publishing date
- 2004
- 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}}, }