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The landscape of viral associations in human cancers

Zapatka, Marc ; Borozan, Ivan ; Brewer, Daniel S ; Iskar, Murat ; Grundhoff, Adam ; Alawi, Malik ; Desai, Nikita ; Sültmann, Holger ; Moch, Holger and Cooper, Colin S , et al. (2020) In Nature Genetics 52(3). p.320-330
Abstract

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,... (More)

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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published
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keywords
DNA Copy Number Variations, DNA Tumor Viruses/genetics, Genome, Human/genetics, Hepatitis B virus/genetics, Herpesvirus 4, Human/genetics, Humans, Mutation, Neoplasms/genetics, Papillomavirus Infections/genetics, Promoter Regions, Genetic/genetics, Telomerase/genetics, Transcriptome, Tumor Virus Infections/virology, Virus Integration
in
Nature Genetics
volume
52
issue
3
pages
320 - 330
publisher
Nature Publishing Group
external identifiers
  • pmid:32025001
  • scopus:85079063026
ISSN
1546-1718
DOI
10.1038/s41588-019-0558-9
language
English
LU publication?
yes
id
1707e5e8-3681-4994-ab58-bc512e1738af
date added to LUP
2023-03-29 19:29:03
date last changed
2024-06-15 03:38:53
@article{1707e5e8-3681-4994-ab58-bc512e1738af,
  abstract     = {{<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 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.</p>}},
  author       = {{Zapatka, Marc and Borozan, Ivan and Brewer, Daniel S and Iskar, Murat and Grundhoff, Adam and Alawi, Malik and Desai, Nikita and Sültmann, Holger and Moch, Holger and Cooper, Colin S and Eils, Roland and Ferretti, Vincent and Lichter, Peter}},
  issn         = {{1546-1718}},
  keywords     = {{DNA Copy Number Variations; DNA Tumor Viruses/genetics; Genome, Human/genetics; Hepatitis B virus/genetics; Herpesvirus 4, Human/genetics; Humans; Mutation; Neoplasms/genetics; Papillomavirus Infections/genetics; Promoter Regions, Genetic/genetics; Telomerase/genetics; Transcriptome; Tumor Virus Infections/virology; Virus Integration}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{320--330}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Nature Genetics}},
  title        = {{The landscape of viral associations in human cancers}},
  url          = {{http://dx.doi.org/10.1038/s41588-019-0558-9}},
  doi          = {{10.1038/s41588-019-0558-9}},
  volume       = {{52}},
  year         = {{2020}},
}