Nutrient-Gene Interactions in Cancer,9780849332296

Nutrient-Gene Interactions in Cancer

by ;
ISBN13: 9780849332296
ISBN10: 084933229X
Format: Hardcover
Pub. Date: 2006-01-24
Publisher(s): CRC Press
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Summary

The complete mapping of the human genome, along with the development of sophisticated molecular technologies, has accelerated research on the relationship between nutrients and genes. This has led to compelling evidence garnered from epidemiological and experimental observations supporting the idea that the interaction between nutrients and genes is one of the most important mechanisms influencing carcinogenesis.Nutrient-Gene Interactions in Cancer brings together leading authorities in the field who provide an overview and look specifically at the mechanisms known to underlie each nutrient and gene interaction. The book examines the multi-functional relationship linking nutrition and cancer development, including the complex role nutrients have in modulating cancer growth via interactions with specific genes, and the emerging new strategy for cancer chemoprevention that is based on a deepened understanding of this relationship. The authors also provide freshly illuminating information on many well-known interactions.The first part of the book includes chapters on the basic elements of biology and pathobiology of gene-nutrient interactions with a focus on mechanisms and biomarkers. This is followed by chapters, which detail specific gene-nutrient interactions, offering numerous examples supported by recent investigations. The final chapter looks to the future, considering the potential for further investigation by outlining new perspectives in this rapidly growing area of medical science.While this work is especially valuable to science investigators, it will also be of great interest to clinicians who manage cancer patients, in that it presents useful tools that advance the clinical value of gene-nutrient interaction research in medical nutrition and oncology.

Table of Contents

Chapter 1 Nutrient and Gene Interactions in Cancer 1(18)
Edward Giovannucci
1.1 Introduction
1(1)
1.2 Types of Epidemiological Studies
1(2)
1.3 Ecological Studies
3(1)
1.4 Analytic Epidemiology: Case—Control and Prospective Cohort Studies
4(3)
1.5 Confounding
7(1)
1.6 Randomized Intervention Trials
8(1)
1.7 The Combined Study of Genetics and Nutrition in Epidemiological Studies
9(4)
1.8 Public Health Implications of Nutrient—Environment Interactions
13(1)
1.9 Summary and Conclusion
14(1)
References
15(4)
Chapter 2 Candidate Mechanisms for Interactions between Nutrients and Genes 19(18)
John C. Mathers
2.1 Introduction
19(1)
2.2 Nutritional Modulation of Gene Expression
20(3)
2.2.1 Effects on Transcription
20(2)
2.2.1.1 Cis-Acting Elements
20(1)
2.2.1.2 Transcription Factors Are Trans-Acting Factors
20(1)
2.2.1.3 Epigenetic Modifications
21(1)
2.2.2 Posttranscriptional Control of Gene Expression
22(1)
2.2.3 Posttranslational Modification
23(1)
2.3 Impact of Genotype on Responses to Nutrients
23(2)
2.4 Mechanisms by which Food Constituents May Influence Carcinogenesis
25(5)
2.4.1 Nutrition, Inflammation, and Cancer Risk
26(12)
2.4.1.1 Intestinal Bacteria
28(1)
2.4.1.2 Obesity
29(1)
2.5 Nutritional Modulation of DNA Damage and Repair
30(1)
2.6 Developmental Origins of Cancer
31(1)
2.7 Concluding Remarks
32(1)
References
33(4)
Chapter 3 Biomarkers for Nutrient–Gene Interactions 37(20)
Claire E. Robertson and Paolo Vineis
3.1 Dietetic Modification of Cancer Risk and Relevant Biomarkers
38(7)
3.1.1 Fruit, Vegetables, and Decreased Cancer Risk: Putative Mechanisms
38(3)
3.1.1.1 Oxidative DNA Damage (8-OHdG)
38(2)
3.1.1.2 Bulky DNA Adducts and Mutagen Sensitivity
40(1)
3.1.2 High Meat Consumption and Increased Risk of Colorectal Cancer
41(1)
3.1.2.1 Heterocyclic Aromatic Amines (HAA) and HAA Adducts
41(1)
3.1.2.2 N-Nitroso Compounds
42(1)
3.1.3 Single Nutrients: Folate
42(5)
3.1.3.1 Evidence and Strength of Association from Cohort Studies
42(3)
3.1.3.2 Alcohol and Folate
45(1)
3.2 Genetic Susceptibility
45(1)
3.3 Combination of Genes and Pathways
46(1)
3.4 Fruit, Vegetables, and Decreased Cancer Risk
47(1)
3.4.1 Hypothesis I: Role of GSTs
47(1)
3.4.2 Hypothesis II: Repair of Oxidative DNA Damage
47(1)
3.5 High Meat Consumption and Increased Risk of Colorectal Cancers
48(1)
3.6 Folate
48(2)
3.6.1 Folate and MTHFR Polymorphisms
48(1)
3.6.2 Folate and Promoter Methylation
49(1)
3.7 Conclusion
50(1)
Acknowledgments
51(1)
Abbreviations
51(1)
References
51(6)
Chapter 4 Interaction between Folate and Methylene-tetrahydrofolate Reductase Gene in Cancer 57(18)
Sang-Woon Choi and Simonetta Friso
4.1 Introduction
57(1)
4.2 Folate and the Risk of Colorectal Cancer
58(2)
4.3 Importance of Folate and MTHFR Gene in One-Carbon Metabolism
60(2)
4.4 Interaction between Folate and MTHFR Gene
62(4)
4.4.1 Characteristics of MTHFR Gene Polymorphisms
62(1)
4.4.2 Mechanism of Folate and MTHFR Gene Interaction
63(1)
4.4.3 Effect of Folate and MTHFR Gene Interaction on DNA Methylation
64(2)
4.5 Interaction between Folate and MTHFR Gene in Colorectal Carcinogenesis
66(1)
4.6 Interaction between Folate and MTHFR Gene in Other Neoplastic Diseases
67(1)
4.7 Conclusion
67(1)
Abbreviations
68(1)
References
69(6)
Chapter 5 Genetic Variability in Folate-Mediated One-Carbon Metabolism and Cancer Risk 75(18)
Cornelia M. Ulrich
5.1 Introduction
75(3)
5.1.1 Investigations of Genetic Variation in Epidemiological Studies
77(1)
5.2 Genetic Variability in One-Carbon Metabolism
78(2)
5.2.1 Thymidylate Synthase (TS)
78(1)
5.2.2 Methionine Synthase (MTR)
78(1)
5.2.3 Methionine Synthase Reductase (MTRR)
79(1)
5.2.4 Serine Hydroxymethyltransferase (SHMT)
79(1)
5.2.5 Cystathionine (3-Synthase (CBS)
79(1)
5.2.6 Reduced Folate Carrier (RFC)
79(1)
5.2.7 Other Genes (GGH, DHFR, and TCII)
80(1)
5.3 Genetic Variability in One-Carbon Metabolism and Cancer Risk
80(4)
5.3.1 Colorectal Cancer
81(2)
5.3.2 Hematopoietic Malignancies
83(1)
5.3.3 Other Cancer Types
83(1)
5.4 Summary
84(1)
Acknowledgment
84(1)
References
84(9)
Chapter 6 S-Adenosylmethionine and Methionine Adenosyltransferase Genes 93(20)
José M. Mato, M. Luz Martinez-Chantar, and Shelly C. Lu
6.1 AdoMet Metabolism
93(1)
6.2 MAT Genes and Their Regulation
94(3)
6.3 AdoMet Regulation of Hepatocyte Growth
97(1)
6.4 AdoMet Regulation of Hepatocyte Apoptosis
98(3)
6.4.1 Differential Effect in Normal vs. Cancerous Hepatocytes
98(1)
6.4.2 AdoMet-Induced Selective Upregulation of Bcl-xs in HepG2 Cells
99(2)
6.5 Consequences of Chronic Hepatic AdoMet Deficiency — the MATIA Knockout Mouse Model
101(4)
6.5.1 Phenotype of the MATIA Null Mice
101(2)
6.5.2 Genomics of MATIA Knockout Mice
103(1)
6.5.3 Proteomics of MATIA Knockout Mice
104(1)
6.5.4 Liver Cancer in MATIA Knockout Mice
105(1)
6.6 Conclusions and Future Directions
105(2)
Acknowledgments
107(1)
Abbreviations
107(1)
References
108(5)
Chapter 7 Effects of Carotenoid Supplementation on Signal Transduction Pathways: Significance in Lung Cancer Prevention 113(16)
Xiang-Dong Wang and Stacey King
7.1 Introduction
113(3)
7.2 Effects of Carotenoid Supplementation on Retinoid Signaling Pathway
116(3)
7.3 Effects of Carotenoid Supplementation on MAPK Pathway
119(1)
7.4 Effects of Carotenoid Supplementation on IGF-1 Signal Transduction Pathway
120(3)
7.5 Conclusion
123(1)
References
124(5)
Chapter 8 The Actions of the Vitamin D Receptor in Health and Malignancy; Polymorphic Associations and Gene Regulatory Actions 129(48)
Moray J. Campbell and Kay W Colston
8.1 Background
130(3)
8.1.1 The Cancer Burden
130(1)
8.1.2 Common and Complex Etiology of Breast, Prostate, and Colon Cancer
130(2)
8.1.3 Emerging Roles of Diet in Malignancy
132(1)
8.2 The Vitamin D Receptor Is a Member of the Nuclear Receptor Superfamily
133(3)
8.2.1 Nuclear Receptors Allow a Local Response to Lipophilic Nutrients
133(2)
8.2.2 Local Remodeling of Chromatin Is Central to Nuclear Receptor Transcriptional Functions
135(1)
8.2.3 Other Functions of VDR That Contribute to Cell Regulatory Actions
136(1)
8.3 The Vitamin D Receptor
136(3)
8.3.1 The VDR: Expressed in a Broad Panel of Noncalcemic Tissues
136(1)
8.3.2 Autocrine vs. Paracrine Signaling
137(1)
8.3.3 VDR Actions in Normal Tissues
138(1)
8.4 Transcriptional and Cellular Effects of the VDR
139(4)
8.4.1 Cell Cycle Progression
140(1)
8.4.2 Programmed Cell Death
140(1)
8.4.3 Adhesion and Migration
141(1)
8.4.4 Genomic Integrity and DNA Repair
142(1)
8.4.5 Integrated Signaling
142(1)
8.5 In Vivo Actions of the VDR in Tumor Models
143(3)
8.5.1 VDR Knockout Tumor Models
143(1)
8.5.2 Other Tumor Models for VDR Actions
144(2)
8.6 Mechanisms of Suppression and Resistance to the Actions of the VDR
146(8)
8.6.1 Reduced Environmental Availability of 1alpha;,25(OH)2D3
146(2)
8.6.2 Cellular Resistance to the Actions of the VDR
148(1)
8.6.3 Genetic Resistance
148(4)
8.6.4 Epigenetic Resistance
152(2)
8.7 Future Perspectives
154(1)
References
154(23)
Chapter 9 The Role of Alcohol Dehydrogenase Polymorphism in Alcohol-Associated Carcinogenesis 177(12)
Helmut K. Seitz and Felix Stickel
9.1 Introduction
177(1)
9.2 Acetaldehyde — a Carcinogen
178(2)
9.3 ALDH2 Mutation and Its Role in Alcohol-Associated Carcinogenesis
180(1)
9.4 Polymorphism of Alcohol Dehydrogenase and Its Possible Role in Alcohol-Associated Carcinogenesis
181(3)
9.4.1 Gastrointestinal Cancer
181(2)
9.4.2 Breast Cancer
183(1)
9.5 Summary and Conclusion
184(1)
References
184(5)
Chapter 10 Genetic Polymorphism of N-Acetyltransferase Genes as Risk Modifiers of Colorectal Cancer from Consumption of Well-Done Meat 189(24)
La Creis Renee Kidd, Robert C.G. Martin, Jason H. Moore, and David W Hein
10.1 Introduction
190(1)
10.2 Heterocyclic Amines
190(1)
10.3 Metabolism of Heterocyclic Amines
191(1)
10.4 Functional Consequences of Variant Metabolic Activation Genes
191(1)
10.5 CYP1A2
192(1)
10.6 N-Acetyltransferase 1 (NAT1)
192(1)
10.7 N-Acetyltransferase 2 (NAT2)
192(2)
10.8 Variant CYP1A2 and N-Acetyltransferase Genes and Their Effect on Colorectal Cancer Risk in Rodents and Humans
194(9)
10.9 CYP1A2 and N-Acetyltransferase Gene Polymorphisms, Alone or in Combination, and Their Effect on Colorectal Cancer Risk among Consumers of Well-Done Meat
203(2)
10.10 Limitations of Gene–Diet Interaction Studies
205(1)
10.11 Future Directions: Strategies to Overcome Sample Size Limitations of Diet–Gene Interaction Studies
206(1)
10.12 The Multifactor Dimensionality Reduction (MDR) Method
206(1)
10.13 Summary
207(1)
References
208(5)
Chapter 11 Ferritin and Serine Hydroxymethyltransferase 213(24)
Patrick J. Stover
11.1 Physiological Role and Regulation of Folate-Mediated One-Carbon Metabolism
213(3)
11.2 Impairments in Folate-Mediated One-Carbon Metabolism
216(1)
11.3 Serine Hydroxymethyltransferase
217(4)
11.3.1 Mitochondrial SHMT
218(1)
11.3.2 Cytoplasmic SHMT
218(5)
11.3.2.1 Serine Synthesis for Gluconeogenesis
218(1)
11.3.2.2 Regulation of Methylene THF Pools
218(1)
11.3.2.3 cSHMT as a Metabolic Switch
219(1)
11.3.2.4 Biosynthesis of 5-Formyl THF
220(1)
11.4 Regulation of cSHMT Expression
221(1)
11.5 Iron–Folate Relationships
222(1)
11.6 Ferritin
222(1)
11.7 Folate–Ferritin Interactions
223(2)
11.7.1 Regulation of Cellular Folate Accumulation
223(2)
11.7.2 Regulation of cSHMT Expression by Ferritin
225(1)
11.8 Folate and Carcinogenesis
225(2)
11.8.1 Mechanism 1: Alteration of DNA Methylation
226(1)
11.8.2 Mechanism 2: Increased Mutation Rates
226(1)
11.9 Future Prospects: HCF and cSHMT Interactions in Cancer Prevention
227(1)
References
228(9)
Chapter 12 Brassica–Gene Interactions and Cancer Risk 237(32)
Jay H. Fowke
12.1 Introduction
238(1)
12.2 Nutritional Epidemiology
239(1)
12.3 Brassica Glucosinolates
240(5)
12.3.1 Glucosinolates
240(1)
12.3.2 Breakdown of Glucosinolates
241(4)
12.4 Phase I Enzymes and Brassica
245(1)
12.4.1 Phase I Enzymes
245(1)
12.4.2 Brassica and Phase I Enzyme Induction
245(1)
12.5 Phase II Enzymes and Brassica
246(1)
12.5.1 Phase II Enzyme System
246(1)
12.5.2 Brassica Phytochemicals and Phase II Enzymes
247(1)
12.5.3 GST Genetic Polymorphisms
247(1)
12.6 ITCs as Phase II Enzyme Substrates
247(1)
12.7 Brassica and Chemical Carcinogenesis
248(1)
12.8 Brassica Consumption, Phase II Enzymes, and Cancer
249(9)
12.8.1 Modification of the Brassica and Cancer Association by Phase II Enzyme Genetic Polymorphisms
250(5)
12.8.1.1 Colon Adenomas or Colon Cancer
250(4)
12.8.1.2 Head and Neck Cancer
254(1)
12.8.1.3 Lung Cancer
254(1)
12.8.2 Possible Limitations of FFQs
255(1)
12.8.3 Brassica Intake Estimated by Urinary ITC Levels
255(1)
12.8.4 Association between Urinary ITC Levels and Cancer by GST Polymorphisms
256(1)
12.8.4.1 Lung Cancer
256(1)
12.8.4.2 Breast Cancer
256(1)
12.8.5 Brassica—Gene Interactions: What Conclusions Are Possible at This Time?
256(2)
12.9 Alternative Mechanisms
258(1)
12.10 Translating Brassica—Cancer Associations to Cancer Prevention
258(1)
12.11 Summary
259(1)
References
259(10)
Chapter 13 Conclusions and Future Perspectives 269(4)
Simonetta Friso, Roberto Corrocher, and Sang-Woon Choi
Index 273

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