Simulation modeling of carcinogenesis

Leon B. Ellwein; Samuel M. Cohen

doi:10.1016/0041-008X(92)90013-I

Simulation modeling of carcinogenesis

Leon B. Ellwein, Samuel M. Cohen

Research output: Contribution to journal › Article › peer-review

15 Scopus citations

Abstract

A discrete-time simulation model of carcinogenesis is described mathematically using recursive relationships between time-varying model variables. The dynamics of cellular behavior is represented within a biological framework that encompasses two irreversible and heritable genetic changes. Empirical data and biological supposition dealing with both control and experimental animal groups are used together to establish values for model input variables. The estimation of these variables is integral to the simulation process as described in step-by-step detail. Hepatocarcinogensis in male F344 rats provides the basis for seven modeling scenarios which illustrate the complexity of relationships among cell proliferation, genotoxicity, and tumor risk.

Original language	English (US)
Pages (from-to)	98-108
Number of pages	11
Journal	Toxicology and Applied Pharmacology
Volume	113
Issue number	1
DOIs	https://doi.org/10.1016/0041-008X(92)90013-I
State	Published - Mar 1992

ASJC Scopus subject areas

Toxicology
Pharmacology

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10.1016/0041-008X(92)90013-I

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title = "Simulation modeling of carcinogenesis",

abstract = "A discrete-time simulation model of carcinogenesis is described mathematically using recursive relationships between time-varying model variables. The dynamics of cellular behavior is represented within a biological framework that encompasses two irreversible and heritable genetic changes. Empirical data and biological supposition dealing with both control and experimental animal groups are used together to establish values for model input variables. The estimation of these variables is integral to the simulation process as described in step-by-step detail. Hepatocarcinogensis in male F344 rats provides the basis for seven modeling scenarios which illustrate the complexity of relationships among cell proliferation, genotoxicity, and tumor risk.",

author = "Ellwein, {Leon B.} and Cohen, {Samuel M.}",

note = "Funding Information: This research is supported in part by USPHS Grants CA325 13, CA44886, and CA36727 from the National Cancer Institute and funding from the International Life Sciences Institute-Nutrition Foundation. We gratefully acknowledge the clerical assistance of Nancy Jensen in the preparation of this manuscript.",

year = "1992",

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AU - Ellwein, Leon B.

AU - Cohen, Samuel M.

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PY - 1992/3

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N2 - A discrete-time simulation model of carcinogenesis is described mathematically using recursive relationships between time-varying model variables. The dynamics of cellular behavior is represented within a biological framework that encompasses two irreversible and heritable genetic changes. Empirical data and biological supposition dealing with both control and experimental animal groups are used together to establish values for model input variables. The estimation of these variables is integral to the simulation process as described in step-by-step detail. Hepatocarcinogensis in male F344 rats provides the basis for seven modeling scenarios which illustrate the complexity of relationships among cell proliferation, genotoxicity, and tumor risk.

AB - A discrete-time simulation model of carcinogenesis is described mathematically using recursive relationships between time-varying model variables. The dynamics of cellular behavior is represented within a biological framework that encompasses two irreversible and heritable genetic changes. Empirical data and biological supposition dealing with both control and experimental animal groups are used together to establish values for model input variables. The estimation of these variables is integral to the simulation process as described in step-by-step detail. Hepatocarcinogensis in male F344 rats provides the basis for seven modeling scenarios which illustrate the complexity of relationships among cell proliferation, genotoxicity, and tumor risk.

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Simulation modeling of carcinogenesis

Abstract

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