Perspectives on Biologically Based Cancer Risk Assessment (häftad)
Format
Häftad (Paperback / softback)
Språk
Engelska
Antal sidor
319
Utgivningsdatum
2012-09-25
Upplaga
Softcover reprint of the original 1st ed. 1999
Förlag
Springer-Verlag New York Inc.
Medarbetare
Cogliano, Vincent James (ed.), Luebeck, E. Georg (ed.), Zapponi, Giovanni A. (ed.)
Illustrationer
XIII, 319 p.
Dimensioner
254 x 178 x 18 mm
Vikt
586 g
Antal komponenter
1
Komponenter
1 Paperback / softback
ISBN
9781461371496
Perspectives on Biologically Based Cancer Risk Assessment (häftad)

Perspectives on Biologically Based Cancer Risk Assessment

Häftad Engelska, 2012-09-25
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The first meeting of the NATO/CCMS Pilot Study "Dose-Response Analysis and Biologically-Based Risk assessment for Initiator and Promoter Carcinogens" was held in Rome, Italy, in the spring of 1991, and was followed by annual or bi-annual meetings held in Germany, Greece, Netherlands, Portugal, USA, up to the end of 1995; in large part supported by NATO/CCMS grants or fellowships, and organized by Pilot Study participants. The Pilot Study activity has been characterized by a higly collaborative atmosphere, which was essential for a deep and detailed analysis of a problem on which different points of view, methodological approaches and regulations exist in the various member countries. The Pilot Study was aimed at proposing a carcinogenic risk assessment procedure which is based on a detailed analysis of the relevant biological processes, and may also consent the verification of hypotheses. The specific form of theoretical and mathe matical models is identified by considering and using the whole set of objective data available. The multidisciplinary approach of the pilot study is reflected by the struc ture of this book. Each chapter is the result of the cooperation of several authors from to produce a comprehensive manual that includes different countries; its objective was both theoretical and practical information.
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Innehållsförteckning

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.-