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Heterogeneity of Cancer Risk Due to Stochastic Effects

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  • Wolfgang F. Heidenreich

Abstract

Persons with exactly the same genetic background, behavior, environment, etc. may have differences in cancer risk due to a different number of cells on the way to malignancy. These differences are estimated quantitatively by using the two‐stage clonal expansion model. For liver cancer the estimated relative risk for persons without intermediate cells at age 40 is less than 10% when compared to the risk of the total population, while the top 0.1% risk group has a more than 100‐fold risk compared to the population. The risk of the 1% percentile in risk is more than 100‐fold of the risk of the more than 95% persons without intermediate cells. The number of intermediate (premalignant) cells in the risk groups cannot be calculated from incidence data only because they depend strongly on a nonidentifiable parameter. But under plausible assumptions, less than about 1,000 intermediate cells are present at age 40 even in high‐risk persons.

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  • Wolfgang F. Heidenreich, 2005. "Heterogeneity of Cancer Risk Due to Stochastic Effects," Risk Analysis, John Wiley & Sons, vol. 25(6), pages 1589-1594, December.
    • Handle: RePEc:wly:riskan:v:25:y:2005:i:6:p:1589-1594
    DOI: 10.1111/j.1539-6924.2005.00685.x
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    References listed on IDEAS

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    1. E. Georg Luebeck & Suresh H. Moolgavkar, 1991. "Stochastic Analysis of Intermediate Lesions in Carcinogenesis Experiments," Risk Analysis, John Wiley & Sons, vol. 11(1), pages 149-157, March.
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    Cited by:

    1. Adam M. Finkel, 2014. "EPA Underestimates, Oversimplifies, Miscommunicates, and Mismanages Cancer Risks by Ignoring Human Susceptibility," Risk Analysis, John Wiley & Sons, vol. 34(10), pages 1785-1794, October.

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