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© 1991 Oxford University Press

research-article

Distinguishing between Models of Carcinogenesis: The Role of Clonal Expansion

ANNETTE KOPP-SCHNEIDER* and CHRISTOPHER J. PORTIER{dagger}

*Abteilung Biostalistik, Institut für Epidemiologie und Biometne Deutsches Krebsforschungszentrwn, Im Neuenheimer Feld 280, D-6900 Heidelberg, Federal Republic of Germany {dagger}Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences PO. Box 12233, Research Triangle Park, North Carolina 27709

Received December 27, 1990; accepted May 6, 1991

Distinguishing between Models of Carcinogenesis: The Role of Clonal Expansion. KOPP-SCHNEIDER, A., AND PORTIER, C. J. (1991). Fundam Appl Toxicol. 17, 601–613. Several multistage models have been proposed to describe the process of carcinogenesis. The model attributed to Armitage and Doll (1954, Brit. J Cancer 8, 1–12) assumes that a normal cell is transformed into a malignant cell by k ≥ 1 fundamental biological events. The model usually attributed to Moolgavkar and colleagues (1979, Math. Biosci 47, 54–77; 1981, J Natltl Cancer Inst 66, 1037–1052) assumes that carcinogenesis is a two-stage process, taking into account the ability of premalignant cells to proliferate. In this paper, we investigate our ability to distinguish between these models using animal carcinogenicity data. Three different approaches are considered: one based on actual tumor incidence data from National Toxicology Program experiments and two based on simulated data. The results show that both models will adequately fit most tumor incidence data. This implies that we must be cautious in accepting the biological basis of either of these models simply because it "fits the data." Suggestions for experimental designs and toxicological endpoints (other than tumor incidence) which might provide for better discrimination between models are given.


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