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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.

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    Authors
    Meyer, Stefan
    Fergusson, William D
    Whetton, Anthony D
    Moreira-Leite, Flavia
    Pepper, Stuart D
    Miller, Crispin J
    Saunders, Emma K
    White, Daniel J
    Will, Andrew M
    Eden, Tim O B
    Ikeda, Hideyuki
    Ullmann, Reinhard
    Tuerkmen, Seval
    Gerlach, Antje
    Klopocki, Eva
    Tönnies, Holger
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    Affiliation
    Academic Unit of Paediatric Oncology, Christie Hospital Trust, University of anchester, Manchester, UK. stefan.meyer@manchester.ac.uk
    Issue Date
    2007-04
    
    Metadata
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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.
    Citation
    Amplification and translocation of 3q26 with overexpression of EVI1 in Fanconi anemia-derived childhood acute myeloid leukemia with biallelic FANCD1/BRCA2 disruption. 2007, 46 (4):359-72 Genes Chromosomes Cancer
    Journal
    Genes, Chromosomes & Cancer
    URI
    http://hdl.handle.net/10541/72886
    DOI
    10.1002/gcc.20417
    PubMed ID
    17243162
    Type
    Article
    Language
    en
    ISSN
    1045-2257
    ae974a485f413a2113503eed53cd6c53
    10.1002/gcc.20417
    Scopus Count
    Collections
    All Christie Publications
    All Paterson Institute for Cancer Research

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