Inhaltsangabe
1. Introduction.- 1.1. Dose-Response Assessment in Nato Countries.- 1.1.1. European Community.- 1.1.1.1. European Union.- 1.1.1.2. The Netherlands.- 1.1.1.3. United Kingdom.- 1.1.1.4. Germany.- 1.1.1.5. Denmark.- 1.1.1.6. Norway.- 1.1.1.7. Other countries.- 1.1.1.8. Concluding remarks.- 1.1.2. United States.- 1.1.2.1. Use of Dose-Response Assessment.- 1.1.2.2. Evolution of Dose-Response Assessment.- 1.1.3. Differences between the United States and European Countries.- 1.2. Future Directions in Dose-Response Assessment.- 1.3. Brief Considerations on Some Commonly Used Parameters.- 1.3.1. Variation in Carcinogenic Potency and in Parameters Adopted for Carcinogen Regulation.- 1.3.2. Toxicity Data and Carcinogenic Potencies: Correlation between Parameters Adopted for Risk Assessment.- 1.3.3. The Linearized Multistage Model and Benchmark Dose (BD) Approaches: Dose-Response Analysis May Provide a Unique Framework for Both the Carcinogenic and Noncarcinogenic Procedures.- 1.4. Structure of this Report.- 1.5. References.- 2. The Biological Basis of Cancer.- 2.1. Introduction.- 2.2. Cell Proliferation.- 2.3. Cell Proliferation and Mutation.- 2.4. Differences in Susceptibility.- 2.5. Mechanisms of Inhibition in Mutagenesis and Carcinogenesis.- 2.5.1. Introduction.- 2.5.2. Inhibition in Mutagenesis and Carcinogenesis.- 2.5.3. Extracellular Inhibition.- 2.5.4. Intracellular Inhibition.- 2.5.5. Inhibitors of Cancer Initiation.- 2.5.6. Inhibitors of Tumor Promotion and Progression.- 2.5.7. Dual Effects of Inhibitors.- 2.6. References.- 3. Sources of Data For Cancer Risk Assessment.- 3.1. Introduction.- 3.2. In Vitro and Short Term Testing.- 3.3. Trends in Animal Toxicology Testing.- 3.4. Cell Proliferation.- 3.4.1. Quantitative Methods and Data Sources.- 3.4.1.1. Direct Measurements of Cell Division.- 3.4.1.2. Serum Biomarkers of Cellular Proliferation.- 3.4.1.3. Cell kinetics of EAF.- 3.5. Sources of Toxicokinetic Data.- 3.5.1. Introduction.- 3.5.2. Model Parameters.- 3.5.2.1. Physiologic.- 3.5.2.2. Biochemical.- 3.5.3. Toxicokinetic Data.- 3.6. Inter- and Intra-Species Variability.- 3.6.1. Variability in Genetic Damage.- 3.6.2. The Parallelogram Model.- 3.7. References.- 4. Use of Biochemical and Molecular Biomarkers For Cancer Risk Assessment in Humans.- 4.1. Introduction.- 4.2. The Initiatory Complex and its Modulators.- 4.2.1. Biomarkers of Exposure.- 4.2.1.1. The External Dose.- 4.2.1.2. The Internal Dose.- 4.2.1.3. The Biologically Effective Dose.- 4.2.1.4. Interaction with Relevant Macromolecules.- 4.2.1.5. Cytogenetic Biomarkers of Early Effects.- 4.2.1.6. Discussion about the Biomarkers of Exposure.- 4.2.2. Biomarkers of Individual Susceptibility.- 4.2.2.1. Phase I Enzymes and Related Markers.- 4.2.2.2. Phase II Enzymes.- 4.2.3. DNA Repair and its Variability.- 4.2.3.1. Assessment of DNA Repair.- 4.2.3.2. Mismatch Repair, Microsatellite Instability and Mutator Phenotype.- 4.2.3.3. Other Genetic Instability Syndromes.- 4.2.3.4. Restatement of the DNA Repair Problem.- 4.2.4. Exogenous Nutritional Factors.- 4.3. The Determinants of the Clonal Expansion of the Initiated Cells.- 4.3.1. Basic Mechanisms.- 4.3.2. Cell Cycle Control Mechanisms.- 4.3.2.1. p53.- 4.3.2.2. The Rb tumour suppressor gene.- 4.3.2.3. The myc Oncogene.- 4.3.2.4. Low Molecular Weight Regulatory Proteins.- 4.3.3. Growth Factors, Growth Factor Receptors and Signal Transduction Pathways.- 4.3.3.1. Growth Factors and Receptors.- 4.3.3.2. Growth Factor Receptors.- 4.3.4. Signal Transduction Pathways.- 4.3.4.1. Transmembrane Receptors with Intrinsic TRK Activity.- 4.3.4.2. Receptors with Seven Transmembrane-spanning Domains.- 4.3.4.3. Cytoskeletal Signal Transduction Pathways.- 4.3.5. The Outcome: The Clonal Expansion of the Initiated Cells.- 4.3.5.1. Proliferation.- 4.3.5.2. Apoptosis.- 4.4. Adjuvant Determinants of the Clonal Expansion.- 4.4.1. Oxidative Damage and its Repair.- 4.4.1.1. Identification of Oxidative Damage.- 4.4.1.2. Thymine Glycol and Thymidine Glycol.-
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