| Literature DB >> 26426381 |
Daniel Martinez1, Alba Navarro, Alejandra Martinez-Trillos, Ricardo Molina-Urra, Blanca Gonzalez-Farre, Itziar Salaverria, Ferran Nadeu, Anna Enjuanes, Guillem Clot, Dolors Costa, Ana Carrio, Neus Villamor, Dolors Colomer, Antonio Martinez, Susanne Bens, Reiner Siebert, Andrew Wotherspoon, Sílvia Beà, Estella Matutes, Elias Campo.
Abstract
Splenic diffuse red pulp small B-cell lymphoma (SDRPL) is considered an indolent neoplasm and its pathogenesis is not well known. We investigated the molecular characteristics of 19 SDRPL patients, 5 of them with progressive disease. IGHV genes were mutated in 9/13 (69%). Cytogenetic and molecular studies identified complex karyotypes in 2 cases, and IGH rearrangements in 3, with PAX5 and potentially TCL1 as partners in each one of them. Copy number arrays showed aberrations in 69% of the tumors, including recurrent losses of 10q23, 14q31-q32, and 17p13 in 3, and 9p21 in 2 cases. Deletion of 7q31.3-q32.3 was present in only 1 case and no trisomies 3 or 18 were detected. NOTCH1 and MAP2K1 were mutated in 2 cases each, whereas BRAF, TP53, and SF3B1 were mutated each in single cases. No mutations were found in NOTCH2 or MYD88. Four of the 5 patients with aggressive disease had mutations in NOTCH1 (2 cases), TP53 (1 case), and MAP2K1 (1 case). The progression-free survival of patients with mutated genes was significantly shorter than in the unmutated (P=0.011). These findings show that SDRPL share some mutated genes but not chromosomal alterations, with other splenic lymphomas, that may confer a more aggressive behavior.Entities:
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Year: 2016 PMID: 26426381 DOI: 10.1097/PAS.0000000000000523
Source DB: PubMed Journal: Am J Surg Pathol ISSN: 0147-5185 Impact factor: 6.394