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Advances in cancer research. Volume 138
- Available as
- Online
Details
- Creator
- edited by Kenneth D. Tew, Paul B. Fisher
- Format
- Books
- Language
- English
- Contributors
- Publication
-
- Cambridge, Massachusetts : Academic Press, 2018
- ©2018
- Physical Details
-
- 1 online resource (239 pages) : illustrations
- ISBNs
- 0128151285, 9780128151280, 9780128151273, 0128151277
- OCLC
- on1029002640
- Includes bibliographical references at the end of each chapters.
- Front Cover -- Advances in Cancer Research -- Copyright -- Contents -- Contributors -- Chapter One: Leveraging Epigenetics to Enhance the Cellular Response to Chemotherapies and Improve Tumor Immunogenicity -- 1. Introduction -- 1.1. Chemotherapy and the Induced Immune Response -- 1.2. The Value of Chemosensitization -- 1.3. Targeting Epigenetics to Achieve Chemosensitization -- 2. Targeting Epigenetic Regulators to Achieve Sensitization to ICD-Inducing Chemotherapies -- 2.1. Writers -- 2.1.1. Histone Acetyltransferases -- 2.1.2. Histone Methyltransferases -- 2.1.3. DNA Methyltransferases -- 2.2. Erasers -- 2.2.1. Histone Deacetylases -- 2.2.2. Histone Demethylases -- 2.2.3. TET Family of DNA Demethylases -- 2.3. Readers -- 2.3.1. Bromodomains -- 2.3.2. Chromodomain Helicase DNA-Binding Proteins -- 2.4. miRNAs -- 3. Conclusions and Future Directions -- Acknowledgments -- Conflicts of Interest -- References -- Chapter Two: VDAC Regulation: A Mitochondrial Target to Stop Cell Proliferation -- 1. Introduction -- 1.1. Mitochondria, Energy Production, and Biosynthesis -- 1.2. Bioenergetics and Biosynthesis in the Warburg Phenotype -- 1.3. Mechanisms to Suppress Mitochondrial ATP Production: A Drive on Glycolysis -- 2. VDAC Channels and Mitochondrial Metabolism -- 2.1. The MOM: A VDAC-Containing Interphase to Modulate Cellular Bioenergetics -- 2.2. VDAC Structure and Regulation of the Conductance -- 3. VDAC-Tubulin Interaction -- 3.1. VDAC Inhibition by Free Tubulin -- 3.2. VDAC-Tubulin Modulation of Cellular Bioenergetics During Cell Cycle -- 4. Tumor Metabolic Flexibility: Advantages of Targeting Metabolism in Chemotherapy -- 5. VDAC-Tubulin Antagonists: A Strategy for Opening VDAC -- 5.1. Erastin and VDAC-Tubulin Antagonists -- 5.2. VDAC Opening, Glycolysis, and Reactive Oxygen Species Formation
- 5.3. VDAC-Dependent Metabolic Hits: Anti-Warburg Effect and Oxidative Stress -- 6. Concluding Remarks -- Acknowledgment -- References -- Chapter Three: Acquired Resistance to Drugs Targeting Tyrosine Kinases -- 1. Introduction -- 2. Inhibition of Bcr-Abl and Nonreceptor Tyrosine Kinases -- 2.1. Mechanisms of Acquired vs Intrinsic Resistance to TKIs -- 2.2. Acquired Resistance to Abl Kinase TKIs -- 3. Receptor and Nonreceptor Tyrosine Kinases Activate Common Pathways -- 4. Receptor TKIs and the EGFR Family -- 4.1. Lapatinib, a Dual Kinase Inhibitor of EGFR and HER2, and Afatinib, a Covalent ErbB1 RTKI -- 4.2. Lapatinib-Induced Kinome Reprogramming and Its Role in Resistance -- 5. Epigenetic Mechanisms of Resistance -- 5.1. Resistance to Receptor TKIs vs Receptor-Targeted Antibodies: IGF-1R -- 5.2. Other mAbs and Acquired Resistance: Trastuzumab -- 6. IGF-1R and Dependence Receptors in Drug Resistance -- 7. Conclusions and Future Perspective -- Acknowledgments -- References -- Chapter Four: Extracellular-Regulated Kinases: Signaling From Ras to ERK Substrates to Control Biological Outcomes -- 1. Introduction -- 2. Identification of Extracellular-Regulated Kinases -- 3. Ras to MAP Kinase Kinases -- 3.1. Ras Activation at the Plasma Membrane -- 3.2. Ras Activation by Sos -- 3.3. Ras Mutational Activation -- 3.4. Rafs -- 3.5. MAP or ERK Kinases (MEKs) -- 4. ERK1 and ERK2 -- 4.1. ERK Activation by Dual Phosphorylation -- 4.2. ERK1 vs ERK2: Who Gets Top Billing? -- 4.3. Cytoplasmic Anchors and Nuclear Translocation -- 4.4. To Dimerization or Not to Dimerize? -- 4.5. Regulation of ERK Activation by Cell Adhesion -- 5. ERK Substrates -- 5.1. Overview of ERK Signaling to Cellular Substrates -- 5.2. Substrate Interaction Domains -- 5.3. Substrate Specificity: Whodunit? -- 5.4. Substrate Identification Techniques -- 5.5. Feedback Phosphorylation
- 5.6. Signaling to Transcription Factors for Cell Proliferation -- 5.7. ERK Signaling to Focal Adhesions -- 5.8. ERK Regulation of RNA Processing -- 5.9. ERK Regulation of Protein Synthesis -- 6. Concluding Remarks -- Acknowledgments -- References -- Chapter Five: Role of MDA-7/IL-24 a Multifunction Protein in Human Diseases -- 1. Introduction -- 2. Characteristic Features of MDA-7/IL-24 -- 2.1. Identification of MDA-7/IL-24 -- 2.2. Structure of MDA-7/IL-24 -- 2.3. Splice Variants/Isoforms of MDA-7/IL-24 -- 2.4. Deletions, Modifications, and Enhancing Stability of MDA-7/IL-24 -- 2.5. Receptors of MDA-7/IL-24 -- 3. Physiological Role of MDA-7/IL-24 -- 3.1. Naturally Occurring Cellular Source of MDA-7/IL-24 -- 3.2. MDA-7/IL-24 Function Under Physiological Conditions -- 4. Functional Role of MDA-7/IL-24 in Cancer -- 4.1. Stem Cells and Differentiation -- 4.2. Apoptosis -- 4.3. Autophagy -- 4.4. Angiogenesis -- 4.5. Invasion and Metastasis -- 4.6. Synergistic Effects -- 4.7. Bystander Activity -- 5. Role of MDA-7/IL-24 in Other Diseases -- 5.1. Inflammation -- 5.2. Inflammatory Bowel Disease (IBD) -- 5.3. Psoriasis -- 5.4. Cardiovascular Disease -- 5.5. Rheumatoid Arthritis (RA) -- 5.6. Tuberculosis -- 5.7. Influenza Virus Replication -- 6. Immunological Effects of MDA-7/IL-24 -- 7. Conclusions and Future Perspectives -- Acknowledgments -- Conflict of Interest -- References -- Chapter Six: Advances and Challenges of HDAC Inhibitors in Cancer Therapeutics -- 1. Histone Deacetylase (HDAC) Inhibitors and Their Targets -- 2. Classes of HDACs -- 3. Lysine Deacylases -- 4. Major Classes of HDAC Inhibitors -- 5. HDAC Inhibitors Have Unique NCI 60 Screening Profiles -- 6. HDAC Inhibitors in the Clinic -- 7. Challenges in Solid Tumor -- 8. Pharmacokinetic Challenges of HDAC Inhibitors
- 9. The History of Hydrazide-Containing Compounds in Clinic and the Future of Next-Generation HDAC Inhibitors -- 10. Conclusion -- References -- Chapter Seven: Prospects of Gene Therapy to Treat Melanoma -- 1. Introduction -- 2. Targets for Gene Therapy -- 3. Gene Therapy in Melanoma -- 4. Challenges of Gene Therapy -- 5. Immunotherapy and Combination Therapy -- 6. Conclusions and Future Directions -- Acknowledgments -- Conflict of Interest -- References -- Back Cover