Richter, Julia and Schlesner, Matthias and Hoffmann, Steve and Kreuz, Markus and Leich, Ellen and Burkhardt, Birgit and Rosolowski, Maciej and Ammerpohl, Ole and Wagener, Rabea and Bernhart, Stephan H. and Lenze, Dido and Szczepanowski, Monika and Paulsen, Maren and Lipinski, Simone and Russell, Robert B. and Adam-Klages, Sabine and Apic, Gordana and Claviez, Alexander and Hasenclever, Dirk and Hovestadt, Volker and Hornig, Nadine and Korbel, Jan O. and Kube, Dieter and Langenberger, David and Lawerenz, Chris and Lisfeld, Jasmin and Meyer, Katharina and Picelli, Simone and Pischimarov, Jordan and Radlwimmer, Bernhard and Rausch, Tobias and Rohde, Marius and Schilhabel, Markus and Scholtysik, Rene and Spang, Rainer and Trautmann, Heiko and Zenz, Thorsten and Borkhardt, Arndt and Drexler, Hans G. and Moeller, Peter and MacLeod, Roderick A. F. and Pott, Christiane and Schreiber, Stefan and Truemper, Lorenz and Loeffler, Markus and Stadler, Peter F. and Lichter, Peter and Eils, Roland and Kueppers, Ralf and Hummel, Michael and Klapper, Wolfram and Rosenstiel, Philip and Rosenwald, Andreas and Brors, Benedikt and Siebert, Reiner (2012) Recurrent mutation of the ID3 gene in Burkitt lymphoma identified by integrated genome, exome and transcriptome sequencing. NATURE GENETICS, 44 (12). pp. 1316-1320. ISSN 1061-4036, 1546-1718
Full text not available from this repository. (Request a copy)Abstract
Burkitt lymphoma is a mature aggressive B-cell lymphoma derived from germinal center B cells(1). Its cytogenetic hallmark is the Burkitt translocation t(8;14)(q24;q32) and its variants, which juxtapose the MYC oncogene with one of the three immunoglobulin loci(2). Consequently, MYC is deregulated, resulting in massive perturbation of gene expression(3). Nevertheless, MYC deregulation alone seems not to be sufficient to drive Burkitt lymphomagenesis. By whole-genome, whole-exome and transcriptome sequencing of four prototypical Burkitt lymphomas with immunoglobulin gene (IG)-MYC translocation, we identified seven recurrently mutated genes. One of these genes, ID3, mapped to a region of focal homozygous loss in Burkitt lymphoma(4). In an extended cohort, 36 of 53 molecularly defined Burkitt lymphomas (68%) carried potentially damaging mutations of ID3. These were strongly enriched at somatic hypermutation motifs. Only 6 of 47 other B-cell lymphomas with the IG-MYC translocation (13%) carried ID3 mutations. These findings suggest that cooperation between ID3 inactivation and IG-MYC translocation is a hallmark of Burkitt lymphomagenesis.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | B-CELL LYMPHOMA; MYC; INACTIVATION; DIAGNOSIS; PROTEINS; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Institut für Funktionelle Genomik > Lehrstuhl für Statistische Bioinformatik (Prof. Spang) |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 04 May 2020 06:00 |
| Last Modified: | 04 May 2020 06:00 |
| URI: | https://pred.uni-regensburg.de/id/eprint/17686 |
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