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Titlebook: Biologically Based Methods for Cancer Risk Assessment; Curtis C. Travis Book 1989 Springer Science+Business Media New York 1989 assessment

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The Hardest Step: Succession Planningdose), and no positive carcinogenicity data have hitherto been obtained. However, the closely related compounds 1,1,2-trichloroethane and 1,1,2,2-tetrachloroethane which are extensively metabolized have produced liver tumors in mice (Baseman et al., 1984).
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https://doi.org/10.1007/978-3-322-85198-7xpression of gene programs in initiated/preneoplastic cells in the liver; inhibition of death of preneoplastic cells by promoters seems to cause rapid growth of preneoplastic lesions. Possible implications for risk assessment are discussed.
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The Epistemology of Mengzian Extension rats, mice or hamsters has been considered to be the most reliable method for the prediction of carcinogenic potential in man (NCI, 1976; IARC, 1980). However, to be internationally accepted these long-term tests must satisfy costly regulatory guidelines for appropriate facilities, long duration (2
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https://doi.org/10.1007/978-1-4020-5265-1ll cultures, 12-0-tetradecanoylphorbol-13-acetate (TPA) enhanced colony formation of rat cells, while it was inhibitory to hamster and human cells (Beeman et al., 1987). We should, therefore, recognize such species-dependent variations and try to understand the mechanisms underlying their occurrence
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The Use of Enzyme-Altered Foci for Risk Assessment of Hepatocarcinogensen the total volume of enzyme-altered tissue in liver and the subsequent development of liver tumors have been established (Emmelot and Scherer, 1980; Kunz et al., 1983, 1985). Enzyme-altered foci are monoclonal in origin (Rabes et al., 1982; Williams et al., 1983) and show a growth advantage over t
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Phenotypic Cellular Changes in Multistage CarcinogenesisIARC, 1986). The diagnosis of foci implies that the altered cell populations are perfectly integrated into the normal architecture of the respective tissue and do not show any expansive growth. At the histological level, preneoplasia may be defined as a phenotypically altered cell population which h
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