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

Détails

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Etat: Public
Version: Final published version
ID Serval
serval:BIB_0D443AB7F882
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Recurrent loss of heterozygosity in 1p36 associated with TNFRSF14 mutations in IRF4 translocation negative pediatric follicular lymphomas.
Périodique
Haematologica
Auteur⸱e⸱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
Statut éditorial
Publié
Date de publication
2013
Volume
98
Numéro
8
Pages
1237-1241
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
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
Oui
Création de la notice
09/08/2013 9:45
Dernière modification de la notice
20/08/2019 12:34
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