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Title: A new recurrent inversion, inv(7)(p15q34), leads to transcriptional activation of HOXA10 and HOXA11 in a subset of T-cell acute lymphoblastic leukemias
Authors: Speleman, F
Cauwelier, B
Dastugue, N
Cools, Jan
Verhasselt, B
Poppe, B
Van Roy, N
Vandesompele, J
Graux, Carlos
Uyttebroeck, Anne
Boogaerts, Marc
De Moerloose, B
Benoit, Y
Selleslag, D
Billiet, J
Robert, A
Huguet, F
Vandenberghe, Peter
De Paepe, A
Marynen, Peter
Hagemeijer-Hausman, Anne # ×
Issue Date: Mar-2005
Publisher: Stockton Press
Series Title: Leukemia vol:19 issue:3 pages:358-366
Abstract: Chromosomal translocations with breakpoints in T-cell receptor (TCR) genes are recurrent in T-cell malignancies. These translocations involve the TCRalphadelta gene (14q11), the TCRbeta gene (7q34) and to a lesser extent the TCRgamma gene at chromosomal band 7p14 and juxtapose T-cell oncogenes next to TCR regulatory sequences leading to deregulated expression of those oncogenes. Here, we describe a new recurrent chromosomal inversion of chromosome 7, inv(7)(p15q34), in a subset of patients with T-cell acute lymphoblastic leukemia characterized by CD2 negative and CD4 positive, CD8 negative blasts. This rearrangement juxtaposes the distal part of the HOXA gene cluster on 7p15 to the TCRbeta locus on 7q34. Real time quantitative PCR analysis for all HOXA genes revealed high levels of HOXA10 and HOXA11 expression in all inv(7) positive cases. This is the first report of a recurrent chromosome rearrangement targeting the HOXA gene cluster in T-cell malignancies resulting in deregulated HOXA gene expression (particularly HOXA10 and HOXA11) and is in keeping with a previous report suggesting HOXA deregulation in MLL-rearranged T- and B cell lymphoblastic leukemia as the key factor in leukaemic transformation. Finally, our observation also supports the previous suggested role of HOXA10 and HOXA11 in normal thymocyte development.
ISSN: 0887-6924
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Molecular Genetics Section (-)
Hematology Section (-)
Clinical Genetics Section (-)
Department of Human Genetics - miscellaneous
Organ Systems (+)
× corresponding author
# (joint) last author

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