Recurrent genomic imbalances in B-cell splenic marginal-zone lymphoma revealed by comparative genomic hybridization

The cytogenetics of splenic marginal zone lymphoma (SMZL) is less well characterized than the cytogenetics of other non-Hodgkin B-cell lymphomas. The aim of this study was to address this issue by identifying characteristic copy number imbalances in SMZL, for which purpose we analyzed 20 SMZL cases...

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Bibliographic Details
Published in:Cancer genetics and cytogenetics 2005-01, Vol.156 (2), p.122-128
Main Authors: Andersen, Claus L., Gruszka-Westwood, Alicja, Atkinson, Shayne, Matutes, Estella, Catovsky, Daniel, Pedersen, Rikke K., Pedersen, Bjarne B., Pulczynski, Stanislaw, Hokland, Peter, Jacobsen, Elisa, Koch, Jørn
Format: Article
Language:English
Subjects:
Adult
Aged
Aged, 80 and over
Chromosome Aberrations
Chromosome Mapping
DNA, Neoplasm - genetics
DNA, Neoplasm - isolation & purification
Humans
In Situ Hybridization, Fluorescence
Lymphoma, B-Cell - genetics
Lymphoma, B-Cell - pathology
Male
Middle Aged
Nucleic Acid Hybridization - methods
Splenic Neoplasms - genetics
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Summary:The cytogenetics of splenic marginal zone lymphoma (SMZL) is less well characterized than the cytogenetics of other non-Hodgkin B-cell lymphomas. The aim of this study was to address this issue by identifying characteristic copy number imbalances in SMZL, for which purpose we analyzed 20 SMZL cases by comparative genomic hybridization (CGH), adding chromosome banding and fluorescence in situ hybridization (FISH) in some cases. CGH identified copy number imbalances in 70% of the cases. Imbalances were recurrently observed for chromosomes 3 (20%), 6 (20%), 7 (25%), 12 (20%), and 14 (10%). The minimally involved regions of these chromosomes were gains of 3q25∼qter and 12q13∼q15, and loss of 6q23, 7q31, and 14q22∼q24. A compilation of our data with data from 3 previous SMZL CGH studies revealed a significant heterogeneity between the studies. Eleven imbalances were recurrently observed in the compiled data set, as opposed to only 5 in our data set. The most frequently observed imbalances in the 73 SMZL cases of the compiled data set were gains of 3q (27%) and 12q (15%), and loss of 7q (18%). Our data suggest that SMZL constitute a genetically heterogeneous disease where gain of 3q25 and loss of 7q31 are the most likely imbalances to be involved in the pathogenesis of the disease.
ISSN:0165-4608
1873-4456
DOI:10.1016/j.cancergencyto.2004.04.026