| Literature DB >> 31738823 |
Joan Enric Ramis-Zaldivar1,2, Blanca Gonzalez-Farré1,2,3, Olga Balagué3, Verónica Celis4, Ferran Nadeu1,2, Julia Salmerón-Villalobos1, Mara Andrés5, Idoia Martin-Guerrero6,7, Marta Garrido-Pontnou8, Ayman Gaafar9, Mariona Suñol10, Carmen Bárcena11, Federico Garcia-Bragado12, Maitane Andión13, Daniel Azorín14, Itziar Astigarraga7, Maria Sagaseta de Ilurdoz15, Constantino Sábado16, Soledad Gallego16, Jaime Verdú-Amorós17, Rafael Fernandez-Delgado17, Vanesa Perez18, Gustavo Tapia19, Anna Mozos20, Montserrat Torrent21, Palma Solano-Páez22, Alfredo Rivas-Delgado3, Ivan Dlouhy3, Guillem Clot1,2, Anna Enjuanes1,2, Armando López-Guillermo3, Pallavi Galera23, Matthew J Oberley24, Alanna Maguire25, Colleen Ramsower25, Lisa M Rimsza26, Leticia Quintanilla-Martinez27, Elaine S Jaffe23, Elías Campo1,2,3, Itziar Salaverria1,2.
Abstract
Pediatric large B-cell lymphomas (LBCLs) share morphological and phenotypic features with adult types but have better prognosis. The higher frequency of some subtypes such as LBCL with IRF4 rearrangement (LBCL-IRF4) in children suggests that some age-related biological differences may exist. To characterize the genetic and molecular heterogeneity of these tumors, we studied 31 diffuse LBCLs (DLBCLs), not otherwise specified (NOS); 20 LBCL-IRF4 cases; and 12 cases of high-grade B-cell lymphoma (HGBCL), NOS in patients ≤25 years using an integrated approach, including targeted gene sequencing, copy-number arrays, and gene expression profiling. Each subgroup displayed different molecular profiles. LBCL-IRF4 had frequent mutations in IRF4 and NF-κB pathway genes (CARD11, CD79B, and MYD88), losses of 17p13 and gains of chromosome 7, 11q12.3-q25, whereas DLBCL, NOS was predominantly of germinal center B-cell (GCB) subtype and carried gene mutations similar to the adult counterpart (eg, SOCS1 and KMT2D), gains of 2p16/REL, and losses of 19p13/CD70. A subset of HGBCL, NOS displayed recurrent alterations of Burkitt lymphoma-related genes such as MYC, ID3, and DDX3X and homozygous deletions of 9p21/CDKN2A, whereas other cases were genetically closer to GCB DLBCL. Factors related to unfavorable outcome were age >18 years; activated B-cell (ABC) DLBCL profile, HGBCL, NOS, high genetic complexity, 1q21-q44 gains, 2p16/REL gains/amplifications, 19p13/CD70 homozygous deletions, and TP53 and MYC mutations. In conclusion, these findings further unravel the molecular heterogeneity of pediatric and young adult LBCL, improve the classification of this group of tumors, and provide new parameters for risk stratification.Entities:
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Year: 2020 PMID: 31738823 PMCID: PMC6978155 DOI: 10.1182/blood.2019002699
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113