Advertisement

Multistage Models for Cancer Risk Assessment

  • Suresh H. Moolgavkar

Abstract

A biologically realistic quantitative model of carcinogenesis is one component of a scientific approach to cancer risk assessment. The parameters of such a model should have clear interpretation in biological terms and, if their dependence on dose of environmental agent can be measured or inferred, then the model can be used for low-dose and inter-species extrapolation of cancer risk.

Keywords

Mutation Rate Hazard Function Intermediate Cell Cancer Risk Assessment Sodium Saccharin 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Armitage, P., and Doll, R., 1954, The age distribution of cancer and a multistage theory of carcinogenesis, Brit. J. Cancer, 8: 1–12.PubMedCrossRefGoogle Scholar
  2. Cavenee, W. K., Dryja, T. P., Phillips, R. A., Benedict, W. F., Godbout, R., Gallie, B. L., Murphree, A. L., Strong, L. C., and White, R. L., 1983, Expression of recessive alleles by chromosomal mechanisms in retinoblastoma, Nature, 305: 779–784.PubMedCrossRefGoogle Scholar
  3. Comings, D. E., 1973, A general theory of carcinogenesis, Proc. Natl. Acad. Sci. U.S.A., 70: 3324–3328.PubMedCrossRefGoogle Scholar
  4. Dewanji, A., Venzon, D. J., and Moolgavkar, S. H., 1988, A stochastic two-stage model for cancer risk assessment I I: The number and size of premalignant clones, Risk Analysis, in Apress.Google Scholar
  5. Ellwein, L. B., and Cohen, S. M., 1988, A cellular dynamics model of experimental bladder cancer: Analysis of the effect of sodium saccharin in the rat, Risk Analysis, in Apress.Google Scholar
  6. Hennings, H., Shores, R., Wenk, M. L., Spangler, E. F., Tarone, R., and Yuspa, S. H., 1983, Malignant conversion of mouse skin tumours is increases by tumour initiators and unaffected by tumour promoters, Nature, 304: 67–69.PubMedCrossRefGoogle Scholar
  7. Hethcote, H. W., and Knudson, A. G., 1978, Model for the incidence of embryonal cancers: Application to retinoblastoma, Proc. Natl. Acad. Sci. U.S.A., 75: 2453–2457.PubMedCrossRefGoogle Scholar
  8. Knudson, A. G., 1971, Mutation, and cancer: Statistical study of retinoblastoma, Proc. Natl. Acad. Sci. U.S.A., 68: 820–823.PubMedCrossRefGoogle Scholar
  9. Knudson, A. G., 1985, Hereditary cancer, oncogenes, and antioncogenes, Cancer Res., 45: 1437–1443.PubMedGoogle Scholar
  10. Knudson, A. G., and Moolgavkar, S. H., 1986, Inherited influences on susceptibility to radiation carcinogenesis, in: “Radiation Carcinogenesis,” A. C. Upton,• ed., Elsevier, North Holland.Google Scholar
  11. Knudson, A. G., Jr., Hethcote, H. W., and Brown, B. W., 1975, Mutation and childhood cancer: A probabilistic model for the incidence of retinoblastoma, Proc. Natl. Acad. Sci. U.S.A., 72: 5116–5120.PubMedCrossRefGoogle Scholar
  12. Koufos, A., Hansen, M. F., Lampkin, B. C., Workman, M. L., Copeland, N. G., Jenkins, N. A., and Cavenee, W. K., 1984, Loss of alleles at loci on human chromosome 11 during genesis of Wilm’s tumour, Nature, 309: 170–172PubMedCrossRefGoogle Scholar
  13. Moolgavkar, S. H., 1986, Carcinogenesis modeling: From molecular biology to epidemiology, Ann. Rev. Publ. Health, 7: 151–169.CrossRefGoogle Scholar
  14. Moolgavkar, S. H., and Dewanji, A., 1988, Biologically-based models for cancer risk assessment: A cautionary note, Risk Analysis, 8: 5–6.PubMedCrossRefGoogle Scholar
  15. Moolgavkar, S. H., and Knudson, A. G., Jr., 1981, Mutation and cancer: A model for human carcinogenesis, J. Natl. Cancer Inst., 66: 1037–1052.PubMedGoogle Scholar
  16. Moolgavkar, S. H., and Venzon, D. J., 1979, Two-event models for carcino-genesis: Incidence curves for childhood and adult tumors, Math. Biosci., 47: 55–77.CrossRefGoogle Scholar
  17. Moolgavkar, S. H., Dewanji, A., and Venzon, D. J., 1988, A stochastic two-stage model for cancer risk assessment I: The hazard function and the probability of tumor, Risk Analysis, in press.Google Scholar
  18. Scherer, E., Feringa, A. W., and Emmelot, P., 1984, Initiation-promotioninitiation, Induction of neoplastic foci within islands of precancerous liver cells in the rat, in: “Models, Mechanisms and Etiology of Tumour Promotion,” M. Börzsönyi, N. E. Day, K. Lapis, and H. Yamasaki, eds., Scherer, E., Feringa, A. W., and Emmelot, P.. 56, Lyon.Google Scholar
  19. Schwarz, M., Pearson, D., Port, R., and Kunz, W., 1984, Promoting effect of 4-dimethylaminoazobenzene on enzyme altered foci induced in rat liver by N-nitrosodiethanolamine, Carcinogenesis, 5: 725–730.PubMedCrossRefGoogle Scholar
  20. Yuspa, S. H., 1984, Mechanisms of initiation and promotion in mouse epidermis, in: “Models, Mechanisms and Etiology of Tumour Promotion,” M. Börzsönyi, N. E. Day, K. Lapis, and H. Yamasaki, eds., Yuspa, S. H.. 56, Lyon.Google Scholar

Copyright information

© Plenum Press, New York 1989

Authors and Affiliations

  • Suresh H. Moolgavkar
    • 1
  1. 1.Fred Hutchinson Cancer Research CenterSeattleUSA

Personalised recommendations