Publications - Published papers
Please find below publications of our group. Currently, we list 565 papers. Some of the publications are in collaboration with the group of Sonja Prohaska and are also listed in the publication list for her individual group. Access to published papers () is restricted to our local network and chosen collaborators.
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Genomic and transcriptomic changes complement each other in the pathogenesis of sporadic Burkitt lymphoma
Lopez, Cristina and Kleinheinz, Kortine and Aukema, Sietse and Rohde, Marius and Bernhart, Stephan H. and Wagener, Rabea and Hübschmann, Daniel and Toprak, Umut and Raimondi, Francesco and Kreuz, Markus and Waszak, Sebastian and Huang, Zhiqin and Sieverling, Lina and Paramasivam, Nagarajan and Seufert, Julian and Sungalee, Stephanie and Russell, Robert and Bausinger, Julia and Kretzmer, Helene and Ammerpohl, Ole and Bergman, Anke and Binder, Hans and Borkhardt, Arndt and Brors, Benedikt and Claviez, Alexander and Doose, Gero and Feuerbach, Lars and Haake, Andrea and Hansmann, Martin-Leo and Höll, Jessica and Hummel, Michael and Korbel, Jan and Lawerenz, Christian and Lenze, Dido and Radlwimmer, Bernhard and Richter, Julia and Rosenstiel, Philip and Rosenwald, Andreas and Schilhabel, Markus and Stein, Harald and Stilgenbauer, Stephan and Stadler, Peter F. and Szczepanowski, Monika and Weniger, Marc and Zapatka, Marc and Eils, Roland and Lichter, Peter and Loeffler, Markus and Moeller, Peter and Trümper Lorenz, and Klapper, Wolfram and Hoffmann, Steve and Kuppers, Ralf and Burkhardt, Birgit and Schlesner, Matthias and Siebert, Reiner
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Status: Published
Nature Comm. 10: 1459
Abstract
Burkitt lymphoma (BL) is the most common B-cell lymphoma in children. Within the International Cancer Genome Consortium (ICGC), we performed whole genome and transcriptome sequencing of 39 sporadic BL. Here, we unravel interaction of structural, mutational, and transcriptional changes, which contribute to MYC oncogene dysregulation together with the pathognomonic IG-MYC translocation. Moreover, by mapping IGH translocation breakpoints, we provide evidence that the precursor of at least a subset of BL is a B-cell poised to express IGHA. We describe the landscape of mutations, structural variants, and mutational processes, and identified a series of driver genes in the pathogenesis of BL, which can be targeted by various mechanisms, including IG-non MYC translocations, germline and somatic mutations, fusion transcripts, and alternative splicing.