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Boffetta, P.* ; Nyberg, F.* ; Mukeria, A.* ; Benhamou, S.* ; Constantinescu, V.* ; Batura-Gabryel, H.* ; Brüske, I. ; Schmid, G.* ; Simonato, L.* ; Pelkonen, P.* ; Hall, J.*

O6-Alkylguanine-DNA-alkyltransferase activity in peripheral leukocytes, smoking and risk of lung cancer.

Cancer Lett. 180, 33-39 (2002)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The level of activity of O6-alkylguanine-DNA-alkyltransferase (AGT), a DNA repair enzyme, in blood lymphocytes may be a marker of susceptibility to lung cancer. We measured the AGT activity level, expressed as pmoles of repaired bases/mg protein, in leukocytes of 153 lung cancer cases (of whom 80 were never smokers) and 106 controls (76 never smokers) enrolled in eight centres from seven countries. Subjects were interviewed with respect to active smoking and exposure to environmental tobacco smoke (ETS). Among never smokers, the odds ratios (ORs) of lung cancer were 1.3 (95% confidence interval 0.5–3.9), 1.5 (0.6–4.1) and 1.4 (0.5–3.8) in quartiles of decreasing AGT activity level, as compared to the upper quartile (P value of test for linear trend 0.6). Corresponding ORs among smokers were 3.4 (0.9–13), 2.0 (0.5–8.3) and 0.4 (0.1–1.6) (P value of test for linear trend 0.4). No interaction was suggested between AGT activity level and either cumulative smoking or exposure to ETS. Reduced AGT activity was not clearly associated with increased lung cancer risk in either smokers or non-smokers. However, the small size of our study argues for a prudent interpretation of our results.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Lung cancer O6-Alkylgualine-DNA-alkyltransferase Tobacco smoking DNA repair Environmental tobacco smoke
Sprache englisch
Veröffentlichungsjahr 2002
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0304-3835
e-ISSN 0304-3835
Zeitschrift Cancer Letters
Quellenangaben Band: 180, Heft: 1, Seiten: 33-39 Artikelnummer: , Supplement: ,
Verlag Elsevier
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Epidemiology (EPI)
Erfassungsdatum 2002-12-31