The landscape of viral associations in human cancers

Marc Zapatka; Ivan Borozan; Daniel S. Brewer; Murat Iskar; Adam Grundhoff; Malik Alawi; Nikita  Desai; Holger Sültmann; Holger Moch; PCAWG Pathogens; Colin S. Cooper; Roland Eils; Vincent Ferretti; Peter Lichter; PCAWG Consortium; Lauri A. Aaltonen; Federico Abascal; Adam Abeshouse; Hiroyuki Aburatani; David J. Adams; Nishant Agrawal; Keun Soo Ahn; Sung-Min Ahn; Hiroshi Aikata; Rehan Akbani; Kadir C. Akdemir; Hikmat Al-Ahmadie; Sultan T. Al-Sedairy; Fatima Al-Shahrour; Malik Alawi; Monique Albert; Kenneth Aldape; Ludmil B. Alexandrov; Adrian Ally; Neil Merrett; et al.

doi:10.1038/s41588-019-0558-9

The landscape of viral associations in human cancers

Marc Zapatka, Ivan Borozan, Daniel S. Brewer, Murat Iskar, Adam Grundhoff, Malik Alawi, Nikita Desai, Holger Sültmann, Holger Moch, PCAWG Pathogens, Colin S. Cooper, Roland Eils, Vincent Ferretti, Peter Lichter, PCAWG Consortium, Lauri A. Aaltonen, Federico Abascal, Adam Abeshouse, Hiroyuki Aburatani, David J. AdamsNishant Agrawal, Keun Soo Ahn, Sung-Min Ahn, Hiroshi Aikata, Rehan Akbani, Kadir C. Akdemir, Hikmat Al-Ahmadie, Sultan T. Al-Sedairy, Fatima Al-Shahrour, Malik Alawi, Monique Albert, Kenneth Aldape, Ludmil B. Alexandrov, Adrian Ally, Neil Merrett, et al.

School of Medicine

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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, 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. There is an author correction to the original article - https://doi.org/10.1038/s41588-023-01316-y

Original language	English
Pages (from-to)	320-330
Number of pages	29
Journal	Nature Genetics
Volume	52
Issue number	3
DOIs	https://doi.org/10.1038/s41588-019-0558-9
Publication status	Published - 1 Mar 2020

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Zapatka, M., Borozan, I., Brewer, D. S., Iskar, M., Grundhoff, A., Alawi, M., Desai, N., Sültmann, H., Moch, H., PCAWG Pathogens, Cooper, C. S., Eils, R., Ferretti, V., Lichter, P., PCAWG Consortium, Aaltonen, L. A., Abascal, F., Abeshouse, A., Aburatani, H., ... et al. (2020). The landscape of viral associations in human cancers. Nature Genetics, 52(3), 320-330. https://doi.org/10.1038/s41588-019-0558-9

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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, 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. There is an author correction to the original article - https://doi.org/10.1038/s41588-023-01316-y",

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Zapatka, M, Borozan, I, Brewer, DS, Iskar, M, Grundhoff, A, Alawi, M, Desai, N, Sültmann, H, Moch, H, PCAWG Pathogens, Cooper, CS, Eils, R, Ferretti, V, Lichter, P, PCAWG Consortium, Aaltonen, LA, Abascal, F, Abeshouse, A, Aburatani, H, Adams, DJ, Agrawal, N, Ahn, KS, Ahn, S-M, Aikata, H, Akbani, R, Akdemir, KC, Al-Ahmadie, H, Al-Sedairy, ST, Al-Shahrour, F, Alawi, M, Albert, M, Aldape, K, Alexandrov, LB, Ally, A, Merrett, N & et al. 2020, 'The landscape of viral associations in human cancers', Nature Genetics, vol. 52, no. 3, pp. 320-330. https://doi.org/10.1038/s41588-019-0558-9

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AU - Zapatka, Marc

AU - Borozan, Ivan

AU - Brewer, Daniel S.

AU - Iskar, Murat

AU - Grundhoff, Adam

AU - Alawi, Malik

AU - Desai, Nikita

AU - Sültmann, Holger

AU - Moch, Holger

AU - PCAWG Pathogens,

AU - Cooper, Colin S.

AU - Eils, Roland

AU - Ferretti, Vincent

AU - Lichter, Peter

AU - PCAWG Consortium,

AU - Aaltonen, Lauri A.

AU - Abascal, Federico

AU - Abeshouse, Adam

AU - Aburatani, Hiroyuki

AU - Adams, David J.

AU - Agrawal, Nishant

AU - Ahn, Keun Soo

AU - Ahn, Sung-Min

AU - Aikata, Hiroshi

AU - Akbani, Rehan

AU - Akdemir, Kadir C.

AU - Al-Ahmadie, Hikmat

AU - Al-Sedairy, Sultan T.

AU - Al-Shahrour, Fatima

AU - Alawi, Malik

AU - Albert, Monique

AU - Aldape, Kenneth

AU - Alexandrov, Ludmil B.

AU - Ally, Adrian

AU - Merrett, Neil

AU - et al.,

PY - 2020/3/1

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N2 - 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. There is an author correction to the original article - https://doi.org/10.1038/s41588-023-01316-y

AB - 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. There is an author correction to the original article - https://doi.org/10.1038/s41588-023-01316-y

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DO - 10.1038/s41588-019-0558-9

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JO - Nature Genetics

JF - Nature Genetics

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ER -

The landscape of viral associations in human cancers

Abstract

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