Chapter
Chapter One: The Role of Advanced Glycation End-Products in Cancer Disparity
2. Advanced Glycation End-Products
3. AGE Metabolites, Lifestyle, and Health Disparity
3.4. Behavioral Risk Factors
3.5. Significance to Ethnic and Racial Health Disparity
4. Mechanisms of AGE Pathogenicity
4.2. Aberrant Cell Signaling
4.2.1. Immune-Mediated Inflammation
5. AGEs, Cancer, and Cancer Disparity
Chapter Two: Disparities in Obesity, Physical Activity Rates, and Breast Cancer Survival
2. Literature Review and Synthesis
2.1. Disparities in Breast Cancer Mortality Rates in the United States
2.2. Relationship Between Weight, Physical Activity, and Breast Cancer Recurrence and Mortality
2.3. Known Biological Mechanisms Link Obesity and Breast Cancer
2.4. Prevalence of Overweight/Obesity and Physical Inactivity in the United States
2.5. Disparities in Overweight/Obesity and Physical Activity in the United States
2.6. Disparities in Overweight/Obesity and Physical Activity in Breast Cancer Survivors
2.7. Evidence-Based Breast Cancer Survivorship Guidelines Related to Physical Activity and Weight Management
3. Conclusions and Future Directions
3.1. Multilevel Intervention Approach to Reduce Obesity (Thereby Reducing Breast Cancer Risk)
3.2. The Social Ecological Model Provides a Basis for Interventions with Multilevel Approaches to Reducing Obesity/Overweight
3.3. Relevance of the SEM for Obesity Reduction Interventions with AA Women Who Are Breast Cancer Survivors
Chapter Three: MicroRNAs and Their Impact on Breast Cancer, the Tumor Microenvironment, and Disparities
1.2. Breast Cancer Disparities
1.4. microRNAs and Cancer
1.5. Circulating microRNAs
1.6. microRNA Therapeutics
2. microRNAs in Breast Cancer Disparities
2.1. Upregulated in AA Women
2.2. Downregulated in AA Women
3. microRNAs in Tumor Microenvironment
4. Summary and Future Perspectives
Chapter Four: Applying a Conceptual Framework to Maximize the Participation of Diverse Populations in Cancer Clinical Trials
2.1. Clinical Trial Participation Barriers Identified in the Conceptual Framework
2.1.1. Awareness Barriers
2.1.2. Opportunity Barriers
2.1.3. Acceptance Barriers
2.1.4. Moderators of Participation in Clinical Trials: Sociodemographic Characteristics
3.1. Case Studies of the Application of the Conceptual Framework
3.1.1. Case Study1: The Selenium and Vitamin E Cancer Prevention Trial (SELECT)
3.1.1.1. Study Design and Results
3.1.1.2. Application of the Conceptual Framework
3.1.1.2.1. Awareness Barriers/Promoters
3.1.1.2.2. Opportunity Barriers/Promoters
3.1.1.2.3. Acceptance Barriers/Promoters
3.1.2. Case Study2: Statewide Cancer Clinical Trial Educational Intervention in South Carolina
3.1.2.1. Study Design and Results
3.1.2.2. Application of the Conceptual Framework
3.1.2.2.1. Awareness Barriers/Promoters
3.1.2.2.2. Opportunity Barriers/Promoters
3.1.2.2.3. Acceptance Barriers/Promoters
3.1.3. Case Study3: Strategies for Recruitment of Minority Patients to Clinical Trials in an Academic Cancer Center in a ...
3.1.3.1. Study Design and Results
3.1.3.2. Application of the Conceptual Framework
3.1.3.2.1. Awareness Barriers/Promoters
3.1.3.2.2. Opportunity Barriers/Promoters
3.1.3.2.3. Acceptance Barriers/Promoters
Chapter Five: Social Networks Across Common Cancer Types: The Evidence, Gaps, and Areas of Potential Impact
3. Cancer, Social Ties, and Social Networks
4. Social Networks in the Digital Age: The Link to Cancer
5. Gender, Cancer, and Social Networks
5.1. Networks Among Women
5.3. Networks and Other Sociodemographic Factors
6. Social Networks and Health Behaviors
6.1. Homophily and Social Networks
8. Potential for Public Health Impact
Chapter Six: Disparities in Cervical Cancer Incidence and Mortality: Can Epigenetics Contribute to Eliminating Disparities?
2. Disparities in Cervical Cancer Incidence and Mortality
3. Disparities in CIN Incidence
6. Cofactors of HPV Infection and CIN Progression
6.1. Poor Adherence to Recommended Care in Ethnic Minorities
6.4. Oral Contraceptive Use
7. HPV Genetics and Epigenetics, and Ethnic Disparities
8.1. Genomically Imprinted Genes Are Epigenetically Labile and Reasonable Candidates
8.2. Deregulation of Imprinted Genes and Human Malignancies
8.3. Malleability of Aberrant Epigenetic Alterations
8.4. Imprinted Gene Networks and Potential Network Deregulation in Progression to Cancer