On the Mechanism of Experimental Carcinogenesis*

Iversen, Simon; Arley, Niels

doi:10.1111/j.1699-0463.1950.tb00081.x

Cited by 76 publications

(7 citation statements)

References 7 publications

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“…He also made the prescient observations that, based on the analysis of Iversen & Arley [19], the number of mutations needed to induce cancer in mice seemed to be less than in humans, and that data on the largely non-epithelial cancers of childhood were not consistent with a model requiring seven mutations. Armitage & Doll [20] tested Nordling's [18] proposal by examining the age-specific incidence of a range of cancers in both sexes [20].…”

Section: Multistage Carcinogenesismentioning

confidence: 99%

Peto's paradox and the promise of comparative oncology

Nunney

Maley

Breen

et al. 2015

Phil. Trans. R. Soc. B

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One contribution of 18 to a theme issue 'Cancer across life: Peto's paradox and the promise of comparative oncology'.Subject Areas: evolution, health and disease and epidemiology, molecular biology, physiology Keywords:Peto's paradox, comparative oncology, evolution, life-history theory, cancer, modelling The past several decades have seen a paradigm shift with the integration of evolutionary thinking into studying cancer. The evolutionary lens is most commonly employed in understanding cancer emergence, tumour growth and metastasis, but there is an increasing realization that cancer defences both between tissues within the individual and between species have been influenced by natural selection. This special issue focuses on discoveries of these deeper evolutionary phenomena in the emerging area of 'comparative oncology'. Comparing cancer dynamics in different tissues or species can lead to insights into how biology and ecology have led to differences in carcinogenesis, and the diversity, incidence and lethality of cancers. In this introduction to the special issue, we review the history of the field and outline how the contributions use empirical, comparative and theoretical approaches to address the processes and patterns associated with 'Peto's paradox', the lack of a statistical relationship of cancer incidence with body size and longevity. This burgeoning area of research can help us understand that cancer is not only a disease but is also a driving force in biological systems and species life histories. Comparative oncology will be key to understanding globally important health issues, including cancer epidemiology, prevention and improved therapies.

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Section: Multistage Carcinogenesismentioning

confidence: 99%

Peto's paradox and the promise of comparative oncology

Nunney

Maley

Breen

et al. 2015

Phil. Trans. R. Soc. B

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“…The probability density per unit time for the appearance of a tumor at time U is (7) 92(u) = flo Xe-lzf(uz) dz = X | e-X(u-z) f(z) dz, and the cumulative probability of a tumor by time t is (8) G2(t) = g0 92(u) du, which reduces to (5). It is clear from the formulation of variant (ii)' that (9) G1(t) > G2(t), since the restriction of attention to the first initiating event means that some tumors which are counted in variant (i) are not counted in variant (ii)'.…”

Section: Mathematical Modelsmentioning

confidence: 99%

“…Variant (ii)' seems implausible, although we have previously followed this approach [7]. Iversen and Arley [8] appear to work with variant (ii)', although their derivation of the distribution of induction period as the result of a stochastic process suggests that variant (i) might be the more appropriate.…”

Section: Mathematical Modelsmentioning

confidence: 99%

“…The model of Iversen and Arley. In a series of papers [8], [11], [13]- [15] Iversen and Arley investigated in considerable detail the particular case of the present model in which F(u) is a cumulative normal distribution, truncated at several standard deviations below the mean. For a constant applied stimulus, X(t) is taken to be constant, while for a single dose of a chemical carcinogen X(t) = Xo exp (-at).…”

Section: Mathematical Modelsmentioning

confidence: 99%

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Stochastic Models of Carcinogenesis

Armitage¹,

Doll²

2015

Series on Concrete and Applicable Mathematics

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“…In part I in this series (Iversen & Arley, 1950, hereafter quoted as I & A ) it was shown that most, if not all, experimental findings regarding carcinogenesis can presumably be interpreted from the point of view of the quantum theoretical >>hit<< theory which has been applied to other biological processes such as e. g. gene-mutations (see e. g. Timofkeff-Ressovsky & Zimmer (1947) or Lea (1946). We also indicated that spontaneously occurring cancer may be explained from this hit theory.…”

Section: Introductionmentioning

confidence: 99%