APOBEC3A/B deletion polymorphism and cancer risk.

Autor:	Gansmo LB; Section of Oncology, Department of Clinical Science, University of Bergen, Bergen, Norway.; Department of Oncology, Haukeland University Hospital, Bergen, Norway., Romundstad P; Department of Public Health, Faculty of Medicine, Trondheim, Norway., Hveem K; Department of Public Health, Faculty of Medicine, K.G. Jebsen Center for Genetic Epidemiology, Norwegian University of Science and Technology, Trondheim, Norway., Vatten L; Department of Public Health, Faculty of Medicine, Trondheim, Norway., Nik-Zainal S; Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK.; Department of Medical Genetics, Addenbrooke's Hospital National Health Service (NHS) Trust, Cambridge, UK., Lønning PE; Section of Oncology, Department of Clinical Science, University of Bergen, Bergen, Norway.; Department of Oncology, Haukeland University Hospital, Bergen, Norway., Knappskog S; Section of Oncology, Department of Clinical Science, University of Bergen, Bergen, Norway.; Department of Oncology, Haukeland University Hospital, Bergen, Norway.
Jazyk:	angličtina
Zdroj:	Carcinogenesis [Carcinogenesis] 2018 Feb 09; Vol. 39 (2), pp. 118-124.
DOI:	10.1093/carcin/bgx131
Abstrakt:	Activity 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. (© The Author(s) 2017. Published by Oxford University Press.)
Databáze:	MEDLINE
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