The landscape of viral associations in human cancers
(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.
(Less)
- author
- contributor
- Borg, Åke LU ; Ringnér, Markus LU and Staaf, Johan LU
- author collaboration
- organization
- publishing date
- 2020-03
- type
- Contribution to journal
- publication status
- published
- subject
- 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
- 2024-07-26 05:17:41
@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}}, }