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  Amplification and translocation of 3q26 with overexpression of EVI1 in Fanconi anemia-derived childhood acute myeloid leukemia with biallelic FANCD1/BRCA2 disruption.

Meyer, S., Fergusson, W. D., Whetton, A. D., Moreira-Leite, F., Pepper, S. D., Miller, C., et al. (2007). Amplification and translocation of 3q26 with overexpression of EVI1 in Fanconi anemia-derived childhood acute myeloid leukemia with biallelic FANCD1/BRCA2 disruption. Genes, Chromosomes and Cancer, 46(4), 359-372. doi:10.1002/gcc.20417.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-820B-5 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-820C-3
Genre: Journal Article
Alternative Title : Genes Chromos Canc

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fulltext_ID=114084239&PLACEBO=IE.pdf (Any fulltext), 757KB
 
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 Creators:
Meyer, Stefan, Author
Fergusson, William D., Author
Whetton, Anthony D., Author
Moreira-Leite, Flavia, Author
Pepper, Stuart D., Author
Miller, Crispin, Author
Saunders, Emma K., Author
White, Daniel J., Author
Will, Andrew M., Author
Eden, Tim, Author
Ikeda, Hideyuki, Author
Ullmann, Reinhard1, Author              
Tuerkmen, Seval2, Author              
Gerlach, Antje, Author
Klopocki, Eva3, Author              
Tönnies, Holger, Author
Affiliations:
1Molecular Cytogenetics (Reinhard Ullmann), Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479645              
2Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433549              
3Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433557              

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 Abstract: Fanconi anemia (FA) is an inherited disease with congenital abnormalities and an extreme risk of acute myeloid leukemia (AML). Genetic events occurring during malignant transformation in FA and the biology of FA-associated AML are poorly understood, but are often preceded by the development of chromosomal aberrations involving 3q26-29 in bone marrow of FA patients. We report here the molecular cytogenetic characterization of FA-derived AML cell lines SB1685CB and SB1690CB by conventional and array comparative genomic hybridization, fluorescence in situ hybridization, and SKY. We identified gains of a 3.7 MB chromosomal region on 3q26.2-26.31, which preceded transformation to overt leukemia. This region harbors the oncogenic transcription factor EVI1. A third FA-derived cell line, FA-AML1, carried a translocation with ectopic localization of 3q26 including EVI1. Rearrangements of 3q, which are rare in childhood AML, commonly result in overexpression of EVI1, which determines specific gene expression patterns and confers poor prognosis. We detected overexpression of EVI1 in all three FA-derived AML. Our results suggest a link between the FA defect, chromosomal aberrations involving 3q and overexpression of EVI1. We hypothesize that constitutional or acquired FA defects might be a common factor for the development of 3q abnormalities in AML. In addition, cryptic imbalances as detected here might account for overexpression of EVI1 in AML without overt 3q26 rearrangements.

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Language(s): eng - English
 Dates: 2007-04-01
 Publication Status: Published in print
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Title: Genes, Chromosomes and Cancer
  Alternative Title : Genes Chromos Canc
Source Genre: Journal
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Pages: - Volume / Issue: 46 (4) Sequence Number: - Start / End Page: 359 - 372 Identifier: ISSN: 1045-2257