Recurrent deletions of the TNFSF7 and TNFSF9 genes in 19p13.3 in diffuse large B-cell and Burkitt lymphomas

A single nucleotide polymorphism‐chip analysis of 98 cases of aggressive B‐cell lymphomas revealed a recurrent deletion at 19p13 in nine of the cases. Six further cases with deletions encompassing this region were found in array‐comparative genomic hybridization data of 295 aggressive B‐cell lymphom...

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Bibliographic Details
Published in:International journal of cancer 2012-09, Vol.131 (5), p.E830-E835
Main Authors: Scholtysik, René, Nagel, Inga, Kreuz, Markus, Vater, Inga, Giefing, Maciej, Schwaenen, Carsten, Wessendorf, Swen, Trümper, Lorenz, Loeffler, Markus, Siebert, Reiner, Küppers, Ralf
Format: Article
Language:English
Subjects:
4-1BB Ligand - genetics
41BBL
Aged
Aged, 80 and over
Burkitt Lymphoma - genetics
Cancer
CD27 Ligand - genetics
CD70
Child
Child, Preschool
Chromosome Mapping
Chromosomes, Human, Pair 19 - genetics
Comparative Genomic Hybridization
diffuse large B-cell lymphoma
DNA, Neoplasm - genetics
Female
Gene Deletion
Gene Expression Regulation, Neoplastic
Genes
Humans
In Situ Hybridization, Fluorescence
Lymphoma
Lymphoma, Large B-Cell, Diffuse - genetics
Male
Medical research
Middle Aged
Oncology
Polymerase Chain Reaction
Polymorphism
Polymorphism, Single Nucleotide
TNFSF7
TNFSF9
tumor suppressor gene
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Summary:A single nucleotide polymorphism‐chip analysis of 98 cases of aggressive B‐cell lymphomas revealed a recurrent deletion at 19p13 in nine of the cases. Six further cases with deletions encompassing this region were found in array‐comparative genomic hybridization data of 295 aggressive B‐cell lymphomas from a previous study. Three cases even showed a homozygous deletion, suggesting a tumor suppressor gene in the deleted region. Two genes encoding members of the tumor necrosis factor superfamily (TNFSF) were located in the minimally deleted region, that is, TNFSF7 and TNFSF9. As no mutations were found within the coding exons of the remaining alleles in the lymphomas with heterozygous deletions, we speculate that the deletions may mostly function through a haploinsufficiency mechanism. The cases with deletions encompassed both diffuse large B‐cell lymphomas and Burkitt lymphomas, and a deletion was also found in a Hodgkin lymphoma cell line. Thus, TNFSF7 and TNFSF9 deletions are recurrent genetic lesions in multiple types of human lymphomas.
ISSN:0020-7136
1097-0215
DOI:10.1002/ijc.27416