Estimates suggest that approximately 35% of cancers are a consequence of suboptimal diet. In this publication, epidemiologists, basic scientists and clinicians review both the epidemiology and mechanistic aspects of nutrition in the prevention of lung, breast, colorectal and prostate cancer. Moreover, an update on the status of the European EPIC study is given. Protein-calorie malnutrition of a clinically significant degree is common among cancer patients and contributes significantly to both morbidity and mortality: Besides causing death solely from progressive cachexia, malnutrition leads to…mehr
Estimates suggest that approximately 35% of cancers are a consequence of suboptimal diet. In this publication, epidemiologists, basic scientists and clinicians review both the epidemiology and mechanistic aspects of nutrition in the prevention of lung, breast, colorectal and prostate cancer. Moreover, an update on the status of the European EPIC study is given. Protein-calorie malnutrition of a clinically significant degree is common among cancer patients and contributes significantly to both morbidity and mortality: Besides causing death solely from progressive cachexia, malnutrition leads to diminished cardiac performance, an increased susceptibility to infection and a diminished response to chemotherapy. Reversing, or even attenuating, this cachexia is an extremely problematic issue. Topics covered here include mechanisms by which malnutrition evolves in cancer patients, animal models of cancer wasting, controversial nutritional interventions in cancer patients and nutritional support in pediatric patients and bone marrow transplantation. It has become clear that 'nutritional oncology' must be regarded as a part of oncology and that it should be integrated with genetics and molecular biology in the care of the cancer patient. This book will appeal to a wide spectrum of professionals concerned with the prevention and treatment of cancer, especially clinical and basic researchers and clinicians.
Produktdetails
Produktdetails
Nestle Nutrition Workshop Series Clinical & Performance Programme
1;Contents;6 2;Preface;8 3;Foreword;12 4;Contributors;14 5;Nutritional Modulation of the Carcinogenesis Process: Targets and Examples;17 5.1;Overview of Multistage Carcinogenesis;17 5.2;Anti-Initiation Strategies: Targets and Examples;19 5.3;Anti-Promotion/Progression Strategies: Targets and Examples;23 5.4;Future Prospects: Transgenic Mouse Models for Nutrition and Cancer Prevention Studies;28 5.5;Conclusions;30 5.6;References;31 5.7;Discussion;34 5.8;References;37 6;Epidemiology of Nutrition and Lung Cancer;39 6.1;Diet and Nutritional Status;40 6.2;Methodological Issues;47 6.3;Conclusion;49 6.4;References;49 6.5;Discussion;51 6.6;Reference;53 7;Antioxidants and Lung Cancer Prevention;55 7.1;Smoke Contains both Carcinogen and Free Radicals Which Can Cause a Variety of Damage to DNA;56 7.2;Controversy Regarding the Chemopreventive Activity of ß-Carotene against Lung Cancer;56 7.3;High-Dose ß-Carotene Supplementation May Result in the Formation of Large Quantities of Undesirable Oxidative Metabolites in the Free Radical-Rich Atmosphere of Lungs of Cigarette Smokers;58 7.4;ß-Carotene Itself Acts as an Anticarcinogen, but Its Oxidized Products Can Facilitate Carcinogenesis;59 7.5;Chronic Smoke Exposure and Excessive ß-Carotene Supplementation Result in Lung Cell Proliferation and Squamous Metaplasia;61 7.6;Adequate Amounts of Vitamin C and Vitamin E Must Be Present to Prevent ß-Carotene from Being Oxidized in Order That ß-Carotene Has a Chemopreventive Effect;66 7.7;Conclusion;67 7.8;References;68 7.9;Discussion;69 8;Prostate Cancer: Epidemiology and Prevention;71 8.1;Laboratory Experiments;72 8.2;Epidemiological Studies and Clinical Trials;72 8.3;Conclusions;76 8.4;References;76 8.5;Discussion;78 8.6;Reference;81 9;Nutrition and Colon Cancer Prevention;83 9.1;Fat and Meat;83 9.2;Fiber;86 9.3;Vegetables and Fruit;88 9.4;Sucrose;90 9.5;Calcium;92 9.6;Vitamin D;93 9.7;Milk Products;93 9.8;Antioxidants and Antioxidant Enzyme-Associated Micronutrients;94 9.9;Folate;96 9.10;Coffee and Tea;97 9.11;Other Aspects;97 9.12;Needed Research;97 9.13;Conclusions;97 9.14;References;100 9.15;Discussion;101 9.16;References;102 10;The Mechanisms by Which Folate Depletion Enhances Colorectal Carcinogenesis: A Unified Scheme;103 10.1;Folate in Nucleic Acid Metabolism;105 10.2;Candidate Mechanisms for Folate-Associated Carcinogenesis;106 10.3;Methylenetetrahydrofolate Reductase and Incidence of Colon Cancer;110 10.4;Conclusion;112 10.5;Acknowledgements;112 10.6;References;112 10.7;Discussion;115 11;Nutrition and Breast Cancer: Epidemiology and Mechanisms;119 11.1;Diet and Breast Cancer Etiology;120 11.2;Diet in Infancy and Childhood and Risk of Breast Cancer;120 11.3;Adult Diet and Risk of Breast Cancer;122 11.4;Conclusions;127 11.5;References;128 11.6;Discussion;131 12;The European Prospective Investigation into Cancer and Nutrition: Perspectives for Cancer Prevention;133 12.1;European Prospective Investigation into Cancer and Nutrition;137 12.2;Conclusions;142 12.3;Acknowledgements;143 12.4;Appendix;143 12.5;References;145 12.6;Discussion;147 12.7;References;149 13;Catabolism of Skeletal Muscle Proteins and Its Reversal in Cancer Cachexia;151 13.1;Model of Cancer Cachexia;152 13.2;Isolation of PIF;153 13.3;Structure and Biological Effect of PIF;154 13.4;Treatment of Cachexia;156 13.5;Clinical Studies;157 13.6;Conclusion;158 13.7;References;158 13.8;Discussion;160 13.9;Reference;162 14;New Mediators in Cancer Cachexia;163 14.1;Malnutrition;164 14.2;Body Weight Loss and Circulating Cytokines;165 14.3;Hypermetabolism;167 14.4;Lipid Metabolism;169 14.5;Muscle Wasting;171 14.6;Acute-Phase Response;173 14.7;Insulin Resistance;174 14.8;Other Mediators;175 14.9;Conclusions;175 14.10;References;177 14.11;Discussion;179 14.12;References;181 15;Animal Models for Nutrition in Cancer;183 15.1;Tumor Model Types;184 15.2;Extrapolation to Humans;187 15.3;Di
1;Contents;6 2;Preface;8 3;Foreword;12 4;Contributors;14 5;Nutritional Modulation of the Carcinogenesis Process: Targets and Examples;17 5.1;Overview of Multistage Carcinogenesis;17 5.2;Anti-Initiation Strategies: Targets and Examples;19 5.3;Anti-Promotion/Progression Strategies: Targets and Examples;23 5.4;Future Prospects: Transgenic Mouse Models for Nutrition and Cancer Prevention Studies;28 5.5;Conclusions;30 5.6;References;31 5.7;Discussion;34 5.8;References;37 6;Epidemiology of Nutrition and Lung Cancer;39 6.1;Diet and Nutritional Status;40 6.2;Methodological Issues;47 6.3;Conclusion;49 6.4;References;49 6.5;Discussion;51 6.6;Reference;53 7;Antioxidants and Lung Cancer Prevention;55 7.1;Smoke Contains both Carcinogen and Free Radicals Which Can Cause a Variety of Damage to DNA;56 7.2;Controversy Regarding the Chemopreventive Activity of ß-Carotene against Lung Cancer;56 7.3;High-Dose ß-Carotene Supplementation May Result in the Formation of Large Quantities of Undesirable Oxidative Metabolites in the Free Radical-Rich Atmosphere of Lungs of Cigarette Smokers;58 7.4;ß-Carotene Itself Acts as an Anticarcinogen, but Its Oxidized Products Can Facilitate Carcinogenesis;59 7.5;Chronic Smoke Exposure and Excessive ß-Carotene Supplementation Result in Lung Cell Proliferation and Squamous Metaplasia;61 7.6;Adequate Amounts of Vitamin C and Vitamin E Must Be Present to Prevent ß-Carotene from Being Oxidized in Order That ß-Carotene Has a Chemopreventive Effect;66 7.7;Conclusion;67 7.8;References;68 7.9;Discussion;69 8;Prostate Cancer: Epidemiology and Prevention;71 8.1;Laboratory Experiments;72 8.2;Epidemiological Studies and Clinical Trials;72 8.3;Conclusions;76 8.4;References;76 8.5;Discussion;78 8.6;Reference;81 9;Nutrition and Colon Cancer Prevention;83 9.1;Fat and Meat;83 9.2;Fiber;86 9.3;Vegetables and Fruit;88 9.4;Sucrose;90 9.5;Calcium;92 9.6;Vitamin D;93 9.7;Milk Products;93 9.8;Antioxidants and Antioxidant Enzyme-Associated Micronutrients;94 9.9;Folate;96 9.10;Coffee and Tea;97 9.11;Other Aspects;97 9.12;Needed Research;97 9.13;Conclusions;97 9.14;References;100 9.15;Discussion;101 9.16;References;102 10;The Mechanisms by Which Folate Depletion Enhances Colorectal Carcinogenesis: A Unified Scheme;103 10.1;Folate in Nucleic Acid Metabolism;105 10.2;Candidate Mechanisms for Folate-Associated Carcinogenesis;106 10.3;Methylenetetrahydrofolate Reductase and Incidence of Colon Cancer;110 10.4;Conclusion;112 10.5;Acknowledgements;112 10.6;References;112 10.7;Discussion;115 11;Nutrition and Breast Cancer: Epidemiology and Mechanisms;119 11.1;Diet and Breast Cancer Etiology;120 11.2;Diet in Infancy and Childhood and Risk of Breast Cancer;120 11.3;Adult Diet and Risk of Breast Cancer;122 11.4;Conclusions;127 11.5;References;128 11.6;Discussion;131 12;The European Prospective Investigation into Cancer and Nutrition: Perspectives for Cancer Prevention;133 12.1;European Prospective Investigation into Cancer and Nutrition;137 12.2;Conclusions;142 12.3;Acknowledgements;143 12.4;Appendix;143 12.5;References;145 12.6;Discussion;147 12.7;References;149 13;Catabolism of Skeletal Muscle Proteins and Its Reversal in Cancer Cachexia;151 13.1;Model of Cancer Cachexia;152 13.2;Isolation of PIF;153 13.3;Structure and Biological Effect of PIF;154 13.4;Treatment of Cachexia;156 13.5;Clinical Studies;157 13.6;Conclusion;158 13.7;References;158 13.8;Discussion;160 13.9;Reference;162 14;New Mediators in Cancer Cachexia;163 14.1;Malnutrition;164 14.2;Body Weight Loss and Circulating Cytokines;165 14.3;Hypermetabolism;167 14.4;Lipid Metabolism;169 14.5;Muscle Wasting;171 14.6;Acute-Phase Response;173 14.7;Insulin Resistance;174 14.8;Other Mediators;175 14.9;Conclusions;175 14.10;References;177 14.11;Discussion;179 14.12;References;181 15;Animal Models for Nutrition in Cancer;183 15.1;Tumor Model Types;184 15.2;Extrapolation to Humans;187 15.3;Di
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