| Literature DB >> 27257180 |
Janine Schmidt1, Shunyou Gong2, Teresa Marafioti3, Barbara Mankel1, Blanca Gonzalez-Farre4, Olga Balagué4, Ana Mozos5, José Cabeçadas6, Jon van der Walt7, Daniela Hoehn8, Andreas Rosenwald9, German Ott10, Stefan Dojcinov11, Caoimhe Egan2, Ferran Nadeu4, Joan Enric Ramis-Zaldívar4, Guillem Clot4, Carmen Bárcena12, Vanesa Pérez-Alonso12, Volker Endris13, Roland Penzel13, Carmen Lome-Maldonado14, Irina Bonzheim1, Falko Fend1, Elias Campo4, Elaine S Jaffe2, Itziar Salaverria4, Leticia Quintanilla-Martinez1.
Abstract
Pediatric-type follicular lymphoma (PTFL) is a variant of follicular lymphoma (FL) with distinctive clinicopathological features. Patients are predominantly young males presenting with localized lymphadenopathy; the tumor shows high-grade cytology and lacks both BCL2 expression and t(14;18) translocation. The genetic alterations involved in the pathogenesis of PTFL are unknown. Therefore, 42 PTFL (40 males and 2 females; mean age, 16 years; range, 5-31) were genetically characterized. For comparison, 11 cases of conventional t(14:18)(-) FL in adults were investigated. Morphologically, PTFL cases had follicular growth pattern without diffuse areas and characteristic immunophenotype. All cases showed monoclonal immunoglobulin (IG) rearrangement. PTFL displays low genomic complexity when compared with t(14;18)(-) FL (mean, 0.77 vs 9 copy number alterations per case; P <001). Both groups presented 1p36 alterations including TNFRSF14, but copy-number neutral loss of heterozygosity (CNN-LOH) of this locus was more frequently observed in PTFL (40% vs 9%; P =075). TNFRSF14 was the most frequently affected gene in PTFL (21 mutations and 2 deletions), identified in 54% of cases, followed by KMT2D mutations in 16%. Other histone-modifying genes were rarely affected. In contrast, t(14;18)(-) FL displayed a mutational profile similar to t(14;18)(+) FL. In 8 PTFL cases (19%), no genetic alterations were identified beyond IG monoclonal rearrangement. The genetic landscape of PTFL suggests that TNFRSF14 mutations accompanied by CNN-LOH of the 1p36 locus in over 70% of mutated cases, as additional selection mechanism, might play a key role in the pathogenesis of this disease. The genetic profiles of PTFL and t(14;18)(-) FL in adults indicate that these are two different disorders.Entities:
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Year: 2016 PMID: 27257180 PMCID: PMC5000845 DOI: 10.1182/blood-2016-03-703819
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113