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Pesch, B.* ; Gawrych, K.* ; Rabstein, S.* ; Weiss, T.* ; Casjens, S.* ; Rihs, H.P.* ; Ding, H.* ; Angerer, J.* ; Illig, T. ; Klopp, N. ; Bueno-de-Mesquita, H.B.* ; Ros, M.M.* ; Kaaks, R.* ; Chang-Claude, J.* ; Roswall, N.* ; Tjønneland, A.* ; Overvad, K.* ; Clavel-Chapelon, F.* ; Boutron-Ruault, M.C.* ; Dossus, L.* ; Boeing, H.* ; Weikert, S.* ; Trichopoulos, D.* ; Palli, D.* ; Sieri, S.* ; Tumino, R.* ; Panico, S.* ; Quirós, J.R.* ; Gonzalez, C.* ; Sánchez, M.J.* ; Dorronsoro, M.* ; Navarro, C.* ; Barricarte, A.* ; Ljungberg, B.* ; Johansson, M.* ; Ulmert, D.* ; Ehrnström, R.* ; Khaw, K.T.* ; Wareham, N.J.* ; Key, T.J.* ; Ferrari, P.* ; Romieu, I.* ; Riboli, E.* ; Brüning, T* ; Vineis, P.*

N-acetyltransferase 2 phenotype, occupation, and bladder cancer risk: Results from the EPIC cohort.

Cancer Epidemiol. Biomarkers Prev. 22, 2055-2065 (2013)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
BACKGROUND: An association between N-acetyltransferase 2 (NAT2) slow acetylation and bladder cancer has been consistently observed in epidemiologic studies. However, evidence has been mainly derived from case-control studies and was sparse from cohort studies. We evaluated the association between NAT2 slow acetylation and bladder cancer in a case-control study nested in the European Prospective Investigation into Cancer and Nutrition. METHODS: Exposure to aromatic amines and polycyclic aromatic hydrocarbons (PAH) could be assessed for 754 cases and 833 controls for whom occupational information was documented. A semiquantitative job-exposure matrix was applied to at-risk occupations to estimate the exposure as low, medium, or high based on tertiles of the distribution of the exposure score in controls. Using a comprehensive genotyping, NAT2 acetylation status could be categorized from 6-single-nucleotide polymorphism genotypes as slow or fast in 607 cases and 695 controls with DNA from archived blood samples. RESULTS: Occupational exposure to aromatic amines and PAH was associated with an increased bladder cancer risk [upper tertile of the distribution of the exposure score: OR = 1.37; 95% confidence interval (CI), 1.02-1.84, and OR = 1.50; 95% CI, 1.09-2.05, respectively]. NAT2 slow acetylation did not modify these risk estimates and was not itself associated with bladder cancer risk (OR = 1.02; 95% CI, 0.81-1.29). CONCLUSIONS: These findings confirm established or suspected occupational risk factors but not the anticipated role of NAT2 slow acetylation in bladder cancer. No interaction was detected between NAT2 and any exposure of interest, including smoking. IMPACT: Genetic testing for NAT2 would be inappropriate in occupational settings.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Nat2 Slow Acetylation ; Polycyclic Aromatic-hydrocarbons ; Gene-environment Interaction ; Urinary-bladder ; Tobacco-smoke ; Gstm1 Null ; Population ; Genotype ; N-acetyltransferase-2 ; Metaanalysis
ISSN (print) / ISBN 1055-9965
e-ISSN 1538-7755
Zeitschrift Cancer Epidemiology, Biomarkers & Prevention
Quellenangaben Band: 22, Heft: 11, Seiten: 2055-2065 Artikelnummer: , Supplement: ,
Verlag American Association for Cancer Research (AACR)
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Research Unit Molecular Epidemiology (AME)