Recurrent loss of heterozygosity in 1p36 associated with TNFRSF14 mutations in IRF4 translocation negative pediatric follicular lymphomas.

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Version: Final published version
Serval ID
serval:BIB_0D443AB7F882
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Recurrent loss of heterozygosity in 1p36 associated with TNFRSF14 mutations in IRF4 translocation negative pediatric follicular lymphomas.
Journal
Haematologica
Author(s)
Martin-Guerrero I., Salaverria I., Burkhardt B., Szczepanowski M., Baudis M., Bens S., de Leval L., Garcia-Orad A., Horn H., Lisfeld J., Pellissery S., Klapper W., Oschlies I., Siebert R.
ISSN
1592-8721 (Electronic)
ISSN-L
0390-6078
Publication state
Published
Issued date
2013
Volume
98
Number
8
Pages
1237-1241
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
Pediatric follicular lymphoma is a rare disease that differs genetically and clinically from its adult counterpart. With the exception of pediatric follicular lymphoma with IRF4-translocation, the genetic events associated with these lymphomas have not yet been defined. We applied array-comparative genomic hybridization and molecular inversion probe assay analyses to formalin-fixed paraffin-embedded tissues from 18 patients aged 18 years and under with IRF4 translocation negative follicular lymphoma. All evaluable cases lacked t(14;18). Only 6 of 16 evaluable cases displayed chromosomal imbalances with gains or amplifications of 6pter-p24.3 (including IRF4) and deletion and copy number neutral-loss of heterozygosity in 1p36 (including TNFRSF14) being most frequent. Sequencing of TNFRSF14 located in the minimal region of loss in 1p36.32 showed nine mutations in 7 cases from our series. Two subsets of pediatric follicular lymphoma were delineated according to the presence of molecular alterations, one with genomic aberrations associated with higher grade and/or diffuse large B-cell lymphoma component and more widespread disease, and another one lacking genetic alterations associated with more limited disease.
Pubmed
Web of science
Open Access
Yes
Create date
09/08/2013 9:45
Last modification date
20/08/2019 12:34
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