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Recurrent deletions of the TNFSF7 and TNFSF9 genes in 19p13.3 in diffuse large B‐cell and Burkitt lymphomas
Author(s) -
Scholtysik René,
Nagel Inga,
Kreuz Markus,
Vater Inga,
Giefing Maciej,
Schwaenen Carsten,
Wessendorf Swen,
Trümper Lorenz,
Loeffler Markus,
Siebert Reiner,
Küppers Ralf
Publication year - 2012
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.27416
Subject(s) - haploinsufficiency , biology , lymphoma , gene , exon , tumor suppressor gene , genetics , burkitt's lymphoma , comparative genomic hybridization , cancer research , microbiology and biotechnology , carcinogenesis , phenotype , chromosome , immunology
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.