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Carcinogenesis Advance Access published online on January 12, 2006
Carcinogenesis, 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
Received July 12, 2005
Revised September 20, 2005
Accepted January 8, 2006

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Analysis of epidemiological cohort data on smoking effects and lung cancer with a multistage cancer model

H. Schöllnberger 1 *, M. Manuguerra 2, H. Bijwaard 1, H. Boshuizen 3, H. P. Altenburg 4, S. M. Rispens 1, M. J. P. Brugmans 1, and P. Vineis 5

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

* To whom correspondence should be addressed.
H. Schöllnberger, E-mail: helmut.schoellnberger{at}sbg.ac.at


  Abstract

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 including 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 ten 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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