http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
Advances in Cancer Research, Volume 138, the latest release in this ongoing, well-regarded serial provides invaluable information on the exciting and fast-moving field of cancer research. This volume presents original reviews on research bridging oncology and gene expression, with this volume covering unconventional approaches to modulating the immunogenicity of tumor cells, tumor dormancy and immunoediting, the emerging role of anti-apoptotic Bcl-2 family proteins in chemoresistance, Beclin-1 and autophagy, MDA-7/IL-24, and nanotechnology and medicine.
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.
edited by Kenneth D. Tew, Paul B. Fisher.