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 Deacetylases2.2.2. 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 Metabolism2.1. 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 Stress6. 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 Resistance5. 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.