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Tumor Microenvironment and Cellular Stress - Constantinos Koumenis

Year 2014


PrefaceChapter 1 Hypoxia and Metabolism in Cancer1.1 Introduction1.1.1 Metabolism in Normal and Cancer Cells1.1.2 Hypoxia and Cancer1.2 Glucose Metabolism1.2.1 Glycolysis in Normal and Cancer Cells1.2.2 The Pentose Phosphate Pathway1.2.3 Hypoxia and Regulation of Glycolysis1.3 Mitochondrial Respiration1.3.1 Mitochondrial Respiration in Normal and Cancer Cells1.3.2 Hypoxia and Mitochondrial Respiration1.4 Glutamine Metabolism1.4.1 Glutaminolysis in Normal and Cancer Cells1.4.2 Interplay Between Glycolysis and Glutaminolysis1.4.3 Hypoxia and Glutaminolysis1.5 Lipid Metabolism1.5.1 Lipid Metabolism in Normal Cells1.5.2 Lipid Metabolism in Cancer Cells1.5.3 Hypoxia and Lipid Metabolism1.6 New Therapeutic Opportunities1.6.1 Targeting Hypoxia1.6.2 Targeting Glucose Metabolism1.6.3 Targeting Glutamine Metabolism1.6.4 Targeting Mitochondrial Function1.6.5 Targeting Lipid Metabolism1.6.6 Metabolic Synthetic Lethality1.7 ConclusionReferencesChapter 2 Hypoxia and Regulation of Cancer Cell Stemness2.1 Introduction2.2 Mechanisms of Hypoxia-Dependent Stemness Regulation2.2.1 Hypoxia-Inducible Factors and Cancer Cell Stemness2.2.2 Hypoxia-Inducible Factors and Stem Cell Gene Expression2.2.3 Other Hypoxia-Regulated Genes and Cancer Stemness2.3 SummaryReferencesChapter 3 Hypoxia-Mediated Metastasis3.1 Metastasis3.2 Hypoxia and Metastasis3.3 Rise of the Metastatic Population3.4 Cancer Cell Invasion3.4.1 Hypoxia and the Epithelial-Mesenchymal Transition3.4.2 Hypoxic Regulation of Invasion3.4.3 Intravasation3.5 The Influence of Hypoxia on Stromal Cells to Promote Tumor Cell Invasion3.6 Survival in Circulation3.7 Homing (Extravasation) and Metastatic Colonization3.7.1 Hypoxia and Extravasation3.7.2 Hypoxia and the Selection of Metastatic Sites3.7.3 Hypoxia and the Premetastatic Niche3.7.4 Hypoxia and Secondary Tumor Growth3.8 Hypoxia and Angiogenesis3.9 ConclusionsReferencesChapter 4 Escape Mechanisms from Antiangiogenic Therapy: An Immune Cell's Perspective4.1 Introduction4.2 Patterns of Resistance to Antiangiogenic Therapy4.3 Innate Immune Cells Facilitate Reneovascularization and Resistance to Antiangiogenic Therapy4.4 ConclusionReferencesChapter 5 Hypoxic VDAC1: A Potential Mitochondrial Marker for Cancer Therapy5.1 Introduction5.2 The Voltage-Dependent Anion Channel5.3 Mitochondrial Phenotype and VDAC5.4 Mitochondria, Metabolism, and Hypoxic VDAC15.5 Mitochondria, Apoptosis, and Hypoxic VDAC15.6 ConclusionReferencesChapter 6 Hypoxia-Directed Drug Strategies to Target the Tumor Microenvironment6.1 Introduction6.1.1 Hypoxia as a Therapeutic Target6.1.2 Drug Development6.1.3 Defining the Hypoxic “Target”6.2 Radiosensitizers6.2.1 Introduction6.2.2 Nitroimidazole Oxygen Mimetics6.2.3 Molecular Targets in DNA Repair as Radiosensitizers6.3 Hypoxia-Activated Prodrugs6.3.1 Introduction6.3.2 PR-1046.3.3 TH-3026.3.4 Tirapazamine6.3.5 Discovery of a Second-Generation Benzotriazine Dioxide (SN30000)6.4 Targeting the Hypoxia Response Pathway6.4.1 Introduction6.4.2 Direct HIF-1α Inhibitors6.4.3 Indirect HIF Inhibitors6.4.4 Targeting Glucose Metabolism6.5 Identifying the Target in Patients6.6 ConclusionsReferencesChapter 7 Radiotherapy and the Tumor Microenvironment: Mutual Influence and Clinical Implications7.1 Introduction7.2 Tumor Hypoxia and Hypoxia-Inducible Factor7.3 Tumor Microvasculature7.4 Diffusible Signaling and the Extracellular Matrix7.5 Stromal Cells7.6 Resident and Infiltrating Immune Cells7.7 Summary and PerspectiveReferencesChapter 8 Autophagy and Cell Death to Target Cancer Cells: Exploiting Synthetic Lethality as Cancer Therapies8.1 Overview of the Autophagy Machinery8.1.1 Autophagosome Formation8.1.2 Maturation of the Autophagosome Through the Endocytic Pathway8.1.3 The End of the Road Through the Lysosome8.2 Role of Autophagy in Cancer8.2.1 Autophagy in Tumor Suppression and Tumor Initiation8.2.2 Autophagy in Tumor Progression8.3 Autophagy and Cell Death as Targets for Anticancer Therapy8.3.1 Autophagy to Induce Cell Death8.3.2 Inhibition of Autophagy to Improve Anticancer Treatments8.4 Synthetic Lethality and Autophagy in Anticancer Drug Discovery8.4.1 Synthetic Lethality in the Context of Cancer8.4.2 Synthetic Lethality and Autophagy in RCC8.5 Conclusion and Future DirectionsReferencesChapter 9 Intratumoral Hypoxia as the Genesis of Genetic Instability and Clinical Prognosis in Prostate Cancer9.1 Clinical Impact of Hypoxia in Prostate Cancer Treatment9.2 Chromosomal Instability and Prostate Cancer Prognosis9.3 Mechanisms for Hypoxia-Mediated Genomic Instability9.3.1 The Effect of Hypoxia on DNA DSB Repair:9.3.2 Other DNA Repair Pathways Modified by Hypoxia: MMR and Nucleotide Excision Repair9.3.3 Using Hypoxia-Mediated DNA Repair Defects9.4 Hypoxia as a Model for Mitotic Control9.4.1 Causes and Consequences of CIN9.4.2 The Effect of Hypoxia on Mitotic Function: A Possible Mechanism of Hypoxia-Induced Genomic Instability9.5 Conclusions and Outstanding QuestionsReferencesChapter 10 miR-210: Fine-Tuning the Hypoxic Response10.1 Introduction10.2 Noncoding RNA: Wide Roles in Physiology and Pathology10.2.1 MicroRNAs10.3 Hypoxia-Regulated miRNAs: The New Paradigm10.3.1 miR-210: A Mirror of HIF Activity with Clinical Implications10.3.2 miR-210 Targets: A Growing and Diverse List10.3.3 miR-210 Regulates Mitochondrial Metabolism and Oxidative Stress10.3.4 miR-210 as a Regulator of Angiogenesis10.3.5 miR-210 Regulation of DNA Damage Response10.3.6 miR-210 Regulation of Apoptosis10.3.7 miR-210 Effects on the Cell Cycle10.3.8 miR-210 as a Candidate Cancer Biomarker10.3.9 miR-210: A Viable Cancer Therapeutic Target?10.4 Concluding RemarksReferencesChapter 11 The Role of Complement in Tumor Growth11.1 The Complement System and Its Regulation11.1.1 The Classical Pathway11.1.2 The Lectin Pathway11.1.3 The Alternative Pathway11.1.4 Nonenzymatic Assembly of the Terminal Pathway Components11.1.5 Alternative Routes of Complement Activation11.1.6 Complement Regulators11.1.7 Opsonization by C3b and Its Related Fragments11.1.8 Biological Effects Mediated by Anaphylatoxins11.2 Cancer Immunity11.3 Complement in Immune Surveillance Against Tumors11.4 Mechanisms for Adaptation and Control of Complement Activation: Implications for Cancer Immunotherapy11.5 Complement Activation Can Promote Carcinogenesis11.5.1 Complement and Immunosuppression11.5.2 Complement and Angiogenesis11.5.3 Complement and Tumor Cell Signaling11.5.4 Complement and Tumor Cell Invasion and Migration11.6 Concluding RemarksReferencesChapter 12 Imaging Angiogenesis, Inflammation, and Metastasis in the Tumor Microenvironment with Magnetic Resonance Imaging12.1 Introduction12.2 Magnetic Resonance Imaging12.3 MRI Methods for Probing Angiogenesis and Tumor Vasculature12.3.1 Dynamic Contrast-Enhanced Measurements of Tumor Vasculature12.3.2 Dynamic Susceptibility Contrast MRI Measurements of Tumor Blood Volume12.3.3 Arterial Spin Labeling Measurements of Tumor Blood Flow12.3.4 Diffusion-Weighted MRI12.4 Molecular and Cellular MRI of Inflammation, Tumor Invasion, and Angiogenesis12.4.1 In Vitro Labeling for Cell Tracking12.4.2 In Vivo Labeling for Cell Tracking and Detection12.4.3 Targeted Contrast Agents for Molecular Imaging12.5 Outlook and ConclusionReferences
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