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This study was supported by the Deutsche Krebshilfe (70-3173-Tr3) through the Network project Molecular Mechanisms in Malignant Lymphomas (from 2003 to 2011); the KinderKrebsInitiative Buchholz/Holm-Seppensen (W. K., R. S.); the International Cancer Genome Consortium MMML-Seq Project funded by the Federal Ministry of Education and Research in Germany within the Program for Medical Genome Research (01KU1002A to 01KU1002J); a fellowship from the Alexander von Humboldt Foundation and the Subprograma Juan de la Cierva Ministerio de Ciencia e Innovacion (JCI-2011-10232) (I. S.); a grant from the Basque Government (Ayuda del programa de perfeccionamiento postdoctoral en el extranjero del Departamento de Educacion, Universidades e Investigacion) (I.M.-G.); a Christoph-Schubert-Award of the KinderKrebsInitiative Buchholz/Holm-Seppensen (R.W.); and Dr Werner Jackstadt Stiftung through a Junior Excellence Research Group (J.R.).

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A recurrent 11q aberration pattern characterizes a subset of MYC-negative high-grade B-cell lymphomas resembling Burkitt lymphoma.

Publicat a:Blood. 123 (8): 1187-1198 - 2014-02-20 123(8), DOI: 10.1182/blood-2013-06-507996

Autors: Salaverria, Itziar; Martin-Guerrero, Idoia; Wagener, Rabea; Kreuz, Markus; Kohler, Christian W; Richter, Julia; Pienkowska-Grela, Barbara; Adam, Patrick; Burkhardt, Birgit; Claviez, Alexander; Damm-Welk, Christine; Drexler, Hans G; Hummel, Michael; Jaffe, Elaine S; Kueppers, Ralf; Lefebvre, Christine; Lisfeld, Jasmin; Loeffler, Markus; Macleod, Roderick A F; Nagel, Inga; Oschlies, Ilske; Rosolowski, Maciej; Russell, Robert B; Rymkiewicz, Grzegorz; Schindler, Detlev; Schlesner, Matthias; Scholtysik, Rene; Schwaenen, Carsten; Spang, Rainer; Szczepanowski, Monika; Truemper, Lorenz; Vater, Inga; Wessendorf, Swen; Siebert, Reiner

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Resum

The genetic hallmark of Burkitt lymphoma (BL) is the t(8;14)(q24;q32) and its variants leading to activation of the MYC oncogene. It is a matter of debate whether true BL without MYC translocation exists. Here, we identified 59 lymphomas concordantly called BL by 2 gene expression classifiers among 753 B-cell lymphomas. Only 2 (3%) of these 59 molecular BL lacked a MYC translocation, which both shared a peculiar pattern of chromosome 11q aberration characterized by interstitial gains including 11q23.2-q23.3 and telomeric losses of 11q24.1-qter. We extended our analysis to 17 MYC-negative high-grade B-cell lymphomas with a similar 11q aberration and showed this aberration to be recurrently associated with morphologic and clinical features of BL. The minimal region of gain was defined by high-level amplifications in 11q23.3 and associated with overexpression of genes including PAFAH1B2 on a transcriptional and protein level. The recurrent region of loss contained a focal homozygous deletion in 11q24.2-q24.3 including the ETS1 gene, which was shown to be mutated in 4 of 16 investigated cases. These findings indicate the existence of a molecularly distinct subset of B-cell lymphomas reminiscent of BL, which is characterized by deregulation of genes in 11q.

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