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Zapatka, Marc; Borozan, Ivan; Brewer, Daniel S.; Iskar, Murat; Grundhoff, Adam; Alawi, Malik; Desai, Nikita; Sültmann, Holger; Moch, Holger; Alawi, Malik; Borozan, Ivan; Brewer, Daniel S.; Cooper, Colin S.; Desai, Nikita; Eils, Roland; Ferretti, Vincent; Grundhoff, Adam; Iskar, Murat; Kleinheinz, Kortine; Lichter, Peter; Nakagawa, Hidewaki; Ojesina, Akinyemi I.; Pedamallu, Chandra Sekhar; Schlesner, Matthias; [...]

The landscape of viral associations in human cancers

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  • Media type: E-Article
  • Title: The landscape of viral associations in human cancers
  • Contributor: Zapatka, Marc; Borozan, Ivan; Brewer, Daniel S.; Iskar, Murat; Grundhoff, Adam; Alawi, Malik; Desai, Nikita; Sültmann, Holger; Moch, Holger; Alawi, Malik; Borozan, Ivan; Brewer, Daniel S.; Cooper, Colin S.; Desai, Nikita; Eils, Roland; Ferretti, Vincent; Grundhoff, Adam; Iskar, Murat; Kleinheinz, Kortine; Lichter, Peter; Nakagawa, Hidewaki; Ojesina, Akinyemi I.; Pedamallu, Chandra Sekhar; Schlesner, Matthias; [...]
  • imprint: Springer Science and Business Media LLC, 2020
  • Published in: Nature Genetics
  • Language: English
  • DOI: 10.1038/s41588-019-0558-9
  • ISSN: 1061-4036; 1546-1718
  • Origination:
  • Footnote:
  • Description: <jats:title>Abstract</jats:title><jats:p>Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, for which whole-genome and—for a subset—whole-transcriptome sequencing data from 2,658 cancers across 38 tumor types was aggregated, we systematically investigated potential viral pathogens using a consensus approach that integrated three independent pipelines. Viruses were detected in 382 genome and 68 transcriptome datasets. We found a high prevalence of known tumor-associated viruses such as Epstein–Barr virus (EBV), hepatitis B virus (HBV) and human papilloma virus (HPV; for example, HPV16 or HPV18). The study revealed significant exclusivity of HPV and driver mutations in head-and-neck cancer and the association of HPV with APOBEC mutational signatures, which suggests that impaired antiviral defense is a driving force in cervical, bladder and head-and-neck carcinoma. For HBV, HPV16, HPV18 and adeno-associated virus-2 (AAV2), viral integration was associated with local variations in genomic copy numbers. Integrations at the <jats:italic>TERT</jats:italic> promoter were associated with high telomerase expression evidently activating this tumor-driving process. High levels of endogenous retrovirus (ERV1) expression were linked to a worse survival outcome in patients with kidney cancer.</jats:p>