The landscape of viral associations in human cancers
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...
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| Hauptverfasser: | , , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
05 February 2020
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| In: |
Nature genetics
Year: 2020, Jahrgang: 52, Heft: 3, Pages: 320-330 |
| ISSN: | 1546-1718 |
| DOI: | 10.1038/s41588-019-0558-9 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/s41588-019-0558-9 Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/s41588-019-0558-9 |
| Verfasserangaben: | Marc Zapatka, Ivan Borozan, Daniel S. Brewer, Murat Iskar, Adam Grundhoff, Malik Alawi, Nikita Desai, Holger Sültmann, Holger Moch, Colin S. Cooper, Roland Eils, Vincent Ferretti, Peter Lichter |
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| 520 | |a 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 TERT 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. | ||
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