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Carcinogenesis Advance Access originally published online on January 12, 2006
Carcinogenesis 2006 27(7):1432-1444; doi:10.1093/carcin/bgi345
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Analysis of epidemiological cohort data on smoking effects and lung cancer with a multi-stage cancer model

H. Schöllnberger *, M. Manuguerra 1, H. Bijwaard, H. Boshuizen 2, H.P. Altenburg 3, S.M. Rispens, M.J.P. Brugmans and P. Vineis 4

RIVM, Laboratory for Radiation Research (LSO), Bilthoven, The Netherlands, 1 ISI Foundation and University of Torino, Italy, 2 RIVM, Centre for Information Technology and Methodology, Bilthoven, The Netherlands, 3 Division of Clinical Epidemiology, Deutsches Krebsforschungszentrum, Heidelberg, Germany and 4 Imperial College London, UK

* To whom correspondence should be addressed at: Helmut Schöllnberger, Department of Molecular Biology, Institute of Physics and Biophysics, University of Salzburg, Hellbrunnerstrasse 34, A-5020 Salzburg, Austria. Tel: +43 662 8044 5709; Fax: +43 662 8044 150; Email: helmut.schoellnberger{at}sbg.ac.at

A stochastic two-stage cancer model is used to analyse the relation between lung cancer and cigarette smoking. The model contains the main rate-limiting stages of carcinogenesis, which include initiation, promotion (clonal expansion of initiated cells), malignant transformation and a lag time for tumour formation. Various data sets were used to test the model. These include the data of a large prospective collaborative project carried out in 10 different European countries, the European Prospective Investigation into Cancer and Nutrition (EPIC). This new data set has not been modelled before. The model is also tested on other published data from CPS-II (Cancer Prevention Study II) of the American Cancer Society and the British doctors' study. The analyses indicate that the EPIC data are best described with smoking dependence on the rates of malignant transformation and clonal expansion. With increasing smoking rates, saturation effects in the two exposure rate-dependent model parameters were observed. The results find confirmation in the biological literature, where both mutational effects and promotional effects of cigarette smoke are documented.


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