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Issues in Risk Assessment (1993)

Chapter: REFERENCES

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Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
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References

Anderson, E.L. and the Carcinogen Assessment Group of the U.S. Environmental Protection Agency. 1983. Quantitative approaches in use to assess cancer risk. Risk Anal. 3:277-295.

Armitage, P., and R. Doll. 1957. A two-stage theory of carcinogenesis in relation to the age distribution of human cancer. Br. J. Cancer 11:161-169.


Balmain, A., and K. Brown. 1988. Oncogene activation in chemical carcinogenesis. Adv. Cancer Res. 51:147-182.

Barbacid, M. 1987. ras genes. Ann. Rev. Biochem. 56:779-827.


Cavender, F.L., B.T. Cook, N.P. Page, V.J. Cogliano, and A.M. Koppibar. 1986. Carcinogenicity Assessment of Chlordane and Heptachlor/heptachlor Epoxide. EPA 600/6-87/004. U.S. Environmental Protection Agency, Research Triangle Park, N.C.

Clement Associates, Inc. 1988. Comparative Potency Approach for Estimating the Cancer Risk Associated with Exposure to Mixtures of Polycyclic Aromatic Hydrocarbons. Interim Final Report. Contract #68-02-4403, prepared for the U.S. Environmental Protection Agency, Research Triangle Park, N.C.

Cohen, S.M., and L.B. Ellwein. 1990. Proliferative and genotoxic cellular effects in 2-acetylaminofluorene bladder and liver carcinogenesis: Biological modeling of the EDO1 study. Toxicol. Appl. Pharmacol. 104:79-93.

Cohen, S.M., and L.B. Ellwein. 1991. Genetic errors, cell prolifera

Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
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tion, and carcinogenesis. Cancer Res. 51:6493-6505.

Cohen, S.M., D.T. Purtilo, and L.B. Ellwein. 1991. Pivotal role of increased cell proliferation in human carcinogenesis. Mod. Pathol. 4:371-382.

Ellwein, L.B., and S.M. Cohen. 1988. A cellular dynamics model of experimental bladder cancer: Analysis of the effect of sodium saccharin in the rat. Risk Anal. 8:215-221.

EPA (U.S. Environmental Protection Agency). 1980. Ambient Water Quality Criteria for Polynuclear Aromatic Hydrocarbons. EPA 440/5-80-069. Environmental Criteria and Assessment Office, Cincinnati, Ohio, and the Office of Water Regulations and Standards, Washington, D.C. Available as NTIS 81-117806.


Gaillie, B.L., J.A. Squire, A. Goddard, J.M. Dunn, M. Canton, D. Hinton, X. Zhu, and R.A. Phillips. 1990. A biology of disease: Mechanisms of oncogenesis in retinoblastoma. Lab. Invest. 62:394-408.

Goyette, M.C., K. Cho, C.L. Fasching, D.B. Levy, K.W. Kinzler, C. Paraskeva, B. Vogelstein, and E.J. Stanbridge. 1992. Progression of colorectal cancer is associated with multiple tumor-suppressor gene defects but inhibition of tumorigenicity is accomplished by correction of any single defect via chromosome transfer. Mol. Cell Biol. 12:1387-1395.

Greenfield, R.E., L.B. Ellwein, and S.M. Cohen. 1984. A general probabilistic model of carcinogenesis: Analysis of experimental urinary bladder cancer. Carcinogenesis 5(4):437-445.


Hollstein, M., D. Sidransky, B. Vogelstein, and C.C. Harris. 1991. p53 mutations in human cancers. Science 253:49-53.


IRDC (International Research and Development Corporation). 1973. Chlordae: Eighteen-month oral carcinogenesis: Analysis of experimental urinary bladder cancer. Report to Velsicol Corporation.


Kopp, A., and C.J. Portier. 1989. A note on approximating the cumulative distribution function of the time to tumor onset in multistage models. Biometr. 45:1259-1263.


Luebeck, E.G., S.H. Moolgavkar, A. Buchman, and M. Schwarz. 1991. Effects of polychlorinated biphenyls in rat liver: Quantitative analysis of enzyme-altered foci. Toxicol. Appl. Pharmacol. 111:469-484.

Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
×

Mantel, N., and W.R. Bryan. 1961. "Safety" testing of carcinogenic agents. J. Natl. Cancer Inst. 27:455-470.

Moolgavkar, S.H. 1988. Biologically motivated two-stage model for cancer risk assessment. Toxicol. Lett. 43(1-3):139-150.

Moolgavkar, S.H., and D.J. Venzon. 1979. Two-event models for carcinogenesis: Incidence curves for childhood and adult tumors. Math. Biosci. 47:55-77.

Moolgavkar, S.H., and A.G. Knudson. 1981. Mutation and cancer: A model for human carcinogenesis. J. Natl. Cancer Inst. 66(6):1037-1052.

Moolgavkar, S.H., and G. Luebeck. 1990. Two-event model for carcinogenesis: Biological, mathematical, and statistical considerations. Risk Anal. 10:323-341.

Moolgavkar, S.H., A. Dewanji, and D.J. Venson. 1988. A stochastic two-stage model for cancer risk assessment. I. The hazard function and the probability of tumor. Risk. Anal. 8:383-392.

Moolgavkar, S.H., E.G. Luebeck, M. de Gunst, R.E. Port, and M. Schwarz. 1990a. Quantitative analysis of enzyme-altered foci in rat hepatocarcinogenesis experiments I: Single agent regimen. Carcinogenesis 11:1271-1278.

Moolgavkar, S.H., F.T. Cross, G. Luebeck, and G.E. Dagle. 1990b. A two-mutation model for radon-induced lung tumors in rats. Radiat. Res. 121:28-37.


NRC (National Research Council). 1983. Risk Assessment in the Federal Government. Washington, D.C.: National Academy Press. 191 pp.

Nebert, D.W. 1989. The Ah locus: Genetic differences in toxicity, cancer, mutation, and birth defects. Crit. Rev. Toxicol. 20:153-174.

Nebert, D.W. 1991a. Polymorphism of human CYP2D genes involved in drug metabolism: Possible relationship to interindividual cancer risk. Cancer Cells 3:93-96.

Nebert, D.W. 1991b. Identification of genetic differences in drug metabolism: Prediction of individual risk of toxicity or cancer. Hepatol. 14:398-401.

Nebert, D.W., D.D. Petersen, and A. Puga. 1991. Human Ah locus polymorphism and cancer: Inducibility of CYPIAI and other genes

Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
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by combustion products and dioxin. Pharmacogen. 1:68-78.

Nebert, D.W., A. Puga, and V. Vasiliou. 1993. Role of the Ah receptor and the dioxin-inducible [Ah] gene battery in toxicity, cancer and in signal transduction. Ann. N.Y. Acad. Sci. (In press)

Portier, C.J. 1987. Statistical properties of a two-stage model of carcinogenesis. Environ. Health Perspect. 76:125-131.

Portier, C.J., and L. Edler. 1990. Two-stage models of carcinogenesis, classification of agents, and design of experiments. Fund. Appl. Toxicol. 14:444-460.


Quinn, D.W. 1989. Calculating the hazard function and probability of tumor for cancer risk assessment when the parameters are time-dependent. Risk Anal. 9:407-413.


Takahashi, T., M.M. Nau, I. Chiba, M.J. Birrer, R.K. Rosenberg, M. Vinocour, M. Levitt, H. Pass, A.F. Gazdar, and J.D. Minna. 1989. p53: A frequent target for genetic abnormalities in lung cancer. Science 246:491-494.

Tan, W.-Y. 1991. Stochastic Models of Carcinogenesis. New York: Marcel Dekker, Inc. 249 pp.

Thorslund, T.W., and G. Charnley. 1988. Quantitative dose-response models for tumor-promoting agents. Pp. 245-256 in Carcinogen Risk Assessment: New Directions in Qualitative and Quantitative Aspects , R.W. Hart and F.D. Hoerger, eds. Banbury Report #31. Cold Spring Harbor Laboratory, Cold Spring Harbor, N.Y.

Thorslund, T.W., C.C. Brown, and G. Charnley. 1987. Biologically motivated cancer risk models. Risk Anal. 7:109-119.

Thyssen, J., J. Althoff, G. Kimmerle, and U. Mohr. 1981. Inhalation studies with benzo[a]pyrene in Syrian golden hamsters. J. Natl. Cancer Inst. 66:575-577.


Williams, G.M., and S. Numoto. 1984. Promotion of mouse liver neoplasms by the oranochlorine pesticides chlordane and heptachlor in comparison to dichlorordiphenyltrichloroethane (DDT). Carcinogenesis 5:1689-1696.

Vogelstein, B., E.R. Fearon, S.R. Hamilton, S.E. Kern, A.C. Preisinger, M. Leppert, Y. Nakamura, R. White, A.M.M. Smits, and J.L. Bos. 1988. Genetic alterations during colorectal-tumor development. N.E. J. Med. 319:525-532.

Weinberg, R.A. 1988. The genetic origin of human cancer. Cancer

Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
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61:1963-1968.

Weinberg, R.A. 1989. Oncogenes, anti-oncogenes and the molecular bases of multistep carcinogenesis. Cancer Res. 49:3713-3721.

Williams, G.M., and S. Numoto. 1984. Promotion of mouse liver neoplasms by the organochlorine pesticides chlordane and heptachlor in comparison to dichlorodiphenyltrichloroethane (DDT). Carcinogenesis 5:1689-1696.

Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
×
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Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
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Page 217
Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
×
Page 218
Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
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Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
×
Page 220
Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
×
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Suggested Citation:"REFERENCES." National Research Council. 1993. Issues in Risk Assessment. Washington, DC: The National Academies Press. doi: 10.17226/2078.
×
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Issues in Risk Assessment Get This Book
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The scientific basis, inference assumptions, regulatory uses, and research needs in risk assessment are considered in this two-part volume.

The first part, Use of Maximum Tolerated Dose in Animal Bioassays for Carcinogenicity, focuses on whether the maximum tolerated dose should continue to be used in carcinogenesis bioassays. The committee considers several options for modifying current bioassay procedures.

The second part, Two-Stage Models of Carcinogenesis, stems from efforts to identify improved means of cancer risk assessment that have resulted in the development of a mathematical dose-response model based on a paradigm for the biologic phenomena thought to be associated with carcinogenesis.

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