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dc.contributor.authorGansmo, Liv B
dc.contributor.authorRomundstad, Paal
dc.contributor.authorHveem, Kristian
dc.contributor.authorVatten, Lars
dc.contributor.authorNik-Zainal, Serena
dc.contributor.authorLønning, Per Eystein
dc.contributor.authorKnappskog, Stian
dc.date.accessioned2018-07-24T14:36:10Z
dc.date.available2018-07-24T14:36:10Z
dc.date.issued2018-02-09
dc.identifier.issn0143-3334
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/278427
dc.description.abstractActivity of the apolipoprotein B mRNA editing enzyme, catalytic-polypeptide-like (APOBEC) enzymes has been linked to specific mutational processes in human cancer genomes. A germline APOBEC3A/B deletion polymorphism is associated with APOBEC-dependent mutational signatures, and the deletion allele has been reported to confer an elevated risk of some cancers in Asian populations, while the results in European populations, so far, have been conflicting. We genotyped the APOBEC3A/B deletion polymorphism in a large population-based sample consisting of 11 106 Caucasian (Norwegian) individuals, including 7279 incident cancer cases (1769 breast, 1360 lung, 1585 colon, and 2565 prostate cancer) and a control group of 3827 matched individuals without cancer (1918 females and 1909 males) from the same population. Overall, the APOBEC3A/B deletion polymorphism was not associated with risk of any of the four cancer types. However, in subgroup analyses stratified by age, we found that the deletion allele was associated with increased risk for lung cancer among individuals <50 years of age (OR 2.17, CI 1.19-3.97), and that the association was gradually reduced with increasing age (P = 0.01). A similar but weaker pattern was observed for prostate cancer. In support of these findings, the APOBEC3A/B deletion was associated with young age at diagnosis among the cancer cases for both cancer forms (lung cancer: P = 0.02; dominant model and prostate cancer: P = 0.03; recessive model). No such associations were observed for breast or colon cancer.
dc.description.sponsorshipThe study was supported by grants from the Bergen Research Foundation, the Norwegian Cancer Society’s Pink Ribbon campaign, the Norwegian Research Council and the Norwegian Health Region West.
dc.languageeng
dc.publisherOxford University Press
dc.rightsAttribution-NonCommercial 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/
dc.titleAPOBEC3A/B deletion polymorphism and cancer risk.
dc.typeArticle
prism.endingPage124
prism.issueIdentifier2
prism.publicationDate2018
prism.publicationNameCarcinogenesis
prism.startingPage118
prism.volume39
dc.identifier.doi10.17863/CAM.25770
dcterms.dateAccepted2017-11-05
rioxxterms.versionofrecord10.1093/carcin/bgx131
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by-nc/4.0/
rioxxterms.licenseref.startdate2018-02-09
dc.contributor.orcidNik-Zainal Abidin, Serena [0000-0001-5054-1727]
dc.identifier.eissn1460-2180
rioxxterms.typeJournal Article/Review
pubs.funder-project-idCancer Research UK (23916)
pubs.funder-project-idCancer Research UK (23433)
cam.issuedOnline2017-11-13


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Attribution-NonCommercial 4.0 International
Except where otherwise noted, this item's licence is described as Attribution-NonCommercial 4.0 International