> Details

López, Cristina; Kleinheinz, Kortine; Aukema, Sietse M.; Rohde, Marius; Bernhart, Stephan H.; Hübschmann, Daniel; Wagener, Rabea; Toprak, Umut H.; Raimondi, Francesco; Kreuz, Markus; Waszak, Sebastian M.; Huang, Zhiqin; Sieverling, Lina; Paramasivam, Nagarajan; Seufert, Julian; Sungalee, Stephanie; Russell, Robert B.; Bausinger, Julia; Kretzmer, Helene; Ammerpohl, Ole; Bergmann, Anke K.; Binder, Hans; Borkhardt, Arndt; Brors, Benedikt; [...]

Genomic and transcriptomic changes complement each other in the pathogenesis of sporadic Burkitt lymphoma

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  • Media type: E-Article
  • Title: Genomic and transcriptomic changes complement each other in the pathogenesis of sporadic Burkitt lymphoma
  • Contributor: López, Cristina; Kleinheinz, Kortine; Aukema, Sietse M.; Rohde, Marius; Bernhart, Stephan H.; Hübschmann, Daniel; Wagener, Rabea; Toprak, Umut H.; Raimondi, Francesco; Kreuz, Markus; Waszak, Sebastian M.; Huang, Zhiqin; Sieverling, Lina; Paramasivam, Nagarajan; Seufert, Julian; Sungalee, Stephanie; Russell, Robert B.; Bausinger, Julia; Kretzmer, Helene; Ammerpohl, Ole; Bergmann, Anke K.; Binder, Hans; Borkhardt, Arndt; Brors, Benedikt; [...]
  • imprint: Springer Science and Business Media LLC, 2019
  • Published in: Nature Communications
  • Language: English
  • DOI: 10.1038/s41467-019-08578-3
  • ISSN: 2041-1723
  • Origination:
  • Footnote:
  • Description: <jats:title>Abstract</jats:title><jats:p>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 <jats:italic>MYC</jats:italic> oncogene dysregulation together with the pathognomonic IG-<jats:italic>MYC</jats:italic> 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 <jats:italic>MYC</jats:italic> translocations, germline and somatic mutations, fusion transcripts, and alternative splicing.</jats:p>
  • Access State: Open Access