Keywords:
Toxicology.
;
Electronic books.
Type of Medium:
Online Resource
Pages:
1 online resource (285 pages)
Edition:
1st ed.
ISBN:
9783319298276
URL:
https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=4534017
DDC:
616.99406
Language:
English
Note:
Intro -- Dedication -- Contents -- Introduction -- Chapter 1: Enhancing the Efficacy of Checkpoint Blockade Through Combination Therapies -- 1 Introduction -- 2 Current Understanding of Mechanisms -- 2.1 CTLA-4 Blockade -- 2.2 PD-1 Pathway Blockade -- 2.3 Additional Coinhibitory Pathways -- 3 Combination Therapies Involving Checkpoint Blockade -- 3.1 Overview of Goals of Rational Combinations with Checkpoint Blockade -- 3.2 Combining Checkpoint Blockade with Other Immunotherapies -- 3.2.1 Targeting Multiple Checkpoint Blockade Agents -- 3.2.2 Targeting T Cell Stimulation -- 3.2.3 T Cell Transfer and Vaccines -- 3.2.4 Targeting Immune Cells Other than T Cells -- 3.3 Combining Checkpoint Blockade with Non-immunotherapies -- 3.3.1 Therapies Targeting Tumor-Specific Mutations -- 3.3.2 Epigenetic Modifiers and Antiangiogenic Agents -- 3.3.3 Radiation Therapy -- 3.3.4 Chemotherapy -- 4 Advancing Combination Checkpoint Therapies -- 4.1 Necessary Next Steps for Advancing Combination Checkpoint Therapies -- 4.2 Understanding Mechanisms of Efficacy of Checkpoint Blockade -- 4.3 Understanding Mechanisms of Resistance to Checkpoint Blockade -- 4.4 Principled Combination of Checkpoint Blockade with Other Immunotherapies -- 4.5 Principled Combination of Checkpoint Blockade with Non-immunotherapies -- 4.6 Using Biomarkers to Predict Response and Stratify Patients -- 4.7 Potential Next-Generation Therapeutic and Diagnostic Strategies -- 5 Future Directions -- References -- Chapter 2: Novel Immunomodulatory Pathways in the Immunoglobulin Superfamily -- 1 Introduction -- 2 CEACAM1 -- 3 ICOS -- 4 LAG-3 -- 5 TIGIT -- 6 TIM-3 -- 7 VISTA -- 8 Summary -- References -- Chapter 3: Parallel Costimulation of Effector and Regulatory T Cells by OX40, GITR, TNFRSF25, CD27, and CD137: Implications for Cancer Immunotherapy -- 1 Introduction -- 2 OX40 (TNFRSF4, CD134).
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3 GITR (TNFRSF18, CD357) -- 4 DR3 (TNFRSF25) -- 5 CD137 (TNFRSF9, 4-1BB) -- 6 CD27 (TNFRSF7) -- 7 Conclusions -- References -- Chapter 4: NK Cell Responses in Immunotherapy: Novel Targets and Applications -- 1 Introduction and NK Cell Basic Biology -- 2 NK Cell Receptors -- 3 The NK Cell Synapse and Cytotoxicity -- 4 NK Cells and Feature of Adaptive Immunity -- 5 NK Cell Migration into Tumors -- 6 How Tumors Evade NK Cells -- 7 Previous Human NK Cell Immunotherapies -- 8 Cytokines -- 9 Adoptive Transfer -- 10 Genetically Modified NK Cells -- 11 Antibodies/ADCC -- 12 CD16 Ehancement -- 13 Anti-KIR -- 14 CD137 -- 15 TLR Agonists -- 16 Checkpoint Inhibitors -- 17 OX40/OX40L -- 18 Elotuzumab -- 19 NK Bispecific Antibodies -- 20 Promising Preclinical Targets -- 20.1 ADAM17 -- 20.2 Chemerin -- 20.3 GSK3 -- 21 Concluding Remarks -- References -- Chapter 5: Reversing T Cell Dysfunction for Tumor Immunotherapy -- 1 T Cells and Tumor Rejection -- 2 T Cell Exhaustion -- 3 Metabolic Dysfunction and T Cell Exhaustion -- 4 Inhibitory Molecules in Antitumor T Cell Regulation -- 4.1 CTLA-4 -- 4.2 PD-1 -- 5 Emerging Inhibitory Checkpoint Receptors: Tim-3 -- 6 Other Emerging Checkpoint Receptors -- 7 Positive Acting (Costimulatory) Checkpoint Receptors as Immunotherapy Targets -- 8 Which Cells Are Being Targeted by ICR Blocking Antibodies? -- 9 Biomarkers for ICR Therapies -- 10 Summary -- References -- Chapter 6: Immunomodulation Within a Single Tumor Site to Induce Systemic Antitumor Immunity: In Situ Vaccination for Cancer -- 1 Introduction -- 2 Manipulation of Intratumoral Myeloid Cells -- 2.1 Increasing the Number of APC at the Tumor Site -- 2.1.1 Autologous DC -- 2.1.2 Allogeneic DC -- 2.1.3 GM-CSF -- 2.1.4 Flt3L -- 2.1.5 Oncolytic Viruses that Increase the Number of APC at the Tumor Site -- 2.2 Activation of APC -- 2.2.1 TLR9 -- 2.2.2 TLR7/8 -- 2.2.3 TLR3.
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2.2.4 TLR4 -- 2.2.5 Live Bacteria -- 2.2.6 Anti-CD40 Monoclonal Antibody -- 2.3 Oncolytic Viruses That Enhance the Cross-presentation of tumor Antigens -- 2.4 Oncolytic Viruses That Increase the Maturation of APCs -- 3 Manipulation of Intratumoral Lymphocytes -- 3.1 Activation of T Cells -- 3.1.1 Interleukin-12 -- 3.1.2 Interleukin-2 -- 3.1.3 T-Cell Activating Oncolytic Viruses -- 3.2 Intratumoral Checkpoint Blockade -- 3.3 Oncolytic Viruses to Reduce Immune Suppression in the Tumor Microenvironment -- 4 Conclusions -- References -- Chapter 7: Novel Targets and Their Assessment for Cancer Treatment -- 1 Drug Discovery in I/O: Can the Promise Become Reality? -- 2 Lessons from the Clinic: How I/O Targets Are Different -- 3 Target Validation in Immune Oncology -- 3.1 The Need for Predictive Translational Datasets -- 3.2 What's Old Is New Again -- 3.3 First-Generation Immune Checkpoint Blockade -- 3.4 PD-1 -- 3.5 The Need to Understand I/O Adverse Events -- 4 Current Tools -- 4.1 The Right Dataset Matters -- 4.2 Response Markers -- 5 Integration: Integrated Profiling at the Single-Cell Level -- 5.1 FACS as the Standard -- 5.2 Mass Spectrometry -- 5.3 NGS -- 5.4 Microengraving -- 5.5 Integration and Response Markers -- 5.6 Power of Human -- References -- Chapter 8: The New Frontier of Antibody Drug Conjugates: Targets, Biology, Chemistry, Payloads -- 1 Introduction -- 2 New Targets for B Cell Leukemias and Lymphomas -- 3 New Targets for the Treatment of Solid Tumors -- 4 Limitations Associated with the Currently Approved ADCs -- 4.1 Conjugation Chemistry Limitations -- 4.2 Molecular Heterogeneity -- 4.3 Warhead Limitations -- 5 Emerging Next-Generation ADC Technologies -- 5.1 Improved Conjugation Chemistry -- 5.2 Addressing Molecular Heterogeneity -- 5.3 Novel Warheads -- 6 Summary -- References.
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Chapter 9: Cellular Therapies: Gene Editing and Next-Gen CAR T Cells -- 1 Introduction -- 2 Engineered Nucleases -- 3 Gene Editing with Cancer Therapeutic Applications -- 3.1 CRISPR for Identifying and Validating Drug Targets -- 3.2 Cancer Model Cell Lines and Animals -- 3.3 Gene Editing for Direct Cancer Therapy -- 4 T Cell Genome Editing for Cell Therapy -- 4.1 CAR T Cell Generations -- 4.2 Other Gene Editing Targets -- 5 Delivery Methods and Vectors -- 5.1 Nonviral Delivery -- 5.1.1 Plasmid DNA Delivery -- 5.1.2 mRNA Delivery -- 5.1.3 Protein Delivery -- 6 Future Generation T Cells -- 6.1 CAR T Cells with Multiple Editing Steps -- 7 Improving Specificity -- 7.1 Improving Transposon Specificity -- 7.2 Altering Recombinases -- 7.3 Changing Viral Integration -- 7.4 Improving Nuclease Delivery -- 7.5 Improving Nuclease Specificity -- 8 Conclusions -- References -- Chapter 10: Targeting the Physicochemical, Cellular, and Immunosuppressive Properties of the Tumor Microenvironment by Depletion of Hyaluronan to Treat Cancer -- 1 Introduction -- 2 Hyaluronan Content in Tumors Is Correlated with Poor Prognosis and More Aggressive Tumor Growth -- 3 Why Does Tumor HA Accumulation Lead to Poor Prognosis and More Aggressive Disease? -- 3.1 Tumor-Cell/Stromal Cell Interactions -- 3.2 Malignancy, Invasiveness, and Migration -- 3.3 HA Accumulation Promotes the Epithelial-Mesenchymal Transition -- 3.4 HA Accumulation Promotes Significant Increases in Tumor Pressure, Decreased Perfusion, and Hypoxia -- 3.5 Impact of HA Accumulation on Immune System Recognition, Dysregulation, and Immunosuppression -- 4 Therapeutic Targeting of HA to Treat Cancer -- 4.1 Determining HA Levels in Tumors -- 4.2 Evidence of Clinical Efficacy with PEGPH20 -- 5 Summary -- References -- Index.
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