Cancer immune therapy : current and future strategies /

Cancer immune therapy : current and future strategies /

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Bibliographic Details
Imprint:Weinheim : Wiley-VCH, c2002.
Description:xxvi, 408 p. : ill. ; 25 cm.
Language:English
Subject:
Neoplasms -- therapy.
Immunotherapy.
Cancer -- Immunotherapy.
Tumors -- Immunological aspects.
Format: Print Book
URL for this record:http://pi.lib.uchicago.edu/1001/cat/bib/4781354
Hidden Bibliographic Details
Other authors / contributors:Stuhler, G. (Gernot)
Walden, Peter, 1954-
ISBN:352730441X (alk. paper)
Notes:Includes bibliographical references and index.
Table of Contents:
  • List of Contributors
  • Color Plates
  • Part 1. Tumor Antigenicity
  • 1. Search for Universal Tumor-Associated T Cell Epitopes
  • 1.1. Introduction
  • 1.2. T Cell Epitopes as the Basis for Anti-Cancer Therapy
  • 1.3. Identification of Tumor-Associated Antigens
  • 1.4. Search for Universal Tumor Antigens
  • 1.5. Epitope Deduction
  • 1.6. Identification of the Telomerase Reverse Transcriptase (hTERT) as a Widely Expressed Tumor-Associated Antigen
  • 1.7. Linking Cancer Genomics to Cancer Immunotherapy
  • 1.8. Prospects for Additional Universal Tumor Antigens
  • 1.9. Prospect of Universal Tumor Antigens as a Clinical Target for Immunotherapy
  • 1.10. Conclusions
  • References
  • 2. Serological Determinants on Tumor Cells
  • 2.1. Introduction
  • 2.2. SEREX: The Approach
  • 2.3. Searching for Human Antigens by SEREX
  • 2.4. Molecular Characterization of SEREX Antigens
  • 2.5. Specificity of SEREX Antigens
  • 2.5.1. Shared Tumor Antigens
  • 2.5.2. Differentiation Antigens
  • 2.5.3. Antigens Encoded by Mutated Genes
  • 2.5.4. Viral Genes
  • 2.5.5. Antigens Encoded by Over-expressed Genes
  • 2.5.6. Amplified Genes
  • 2.5.7. Splice Variants of Known Genes
  • 2.5.8. Cancer-Related Autoantigens
  • 2.5.9. Non-Cancer-Related Autoantigens
  • 2.5.10. Products of Underexpressed Genes
  • 2.6. Incidence of Antibodies to SEREX Antigens and Clinical Significance
  • 2.7. Functional Significance of SEREX Antigens
  • 2.8. Reverse T Cell Immunology
  • 2.9. Towards a Definition of the Human Cancer Immunome
  • 2.10. Consequences for Cancer Vaccine Development
  • 2.11. Conclusions and Perspectives
  • References
  • 3. Processing and Presentation of Tumor-associated Antigens
  • 3.1. The Major Histocompatibility Complex (MHC) Class I Antigen-Processing Pathway
  • 3.2. Immuno-Proteasomes
  • 3.2.1. The Function of Immuno-Proteasomes
  • 3.2.2. The Role of the Proteasome Activator PA28 in Antigen Processing
  • 3.3. The Proteasome System and Tumor Antigen Presentation
  • 3.3.1. Impaired Epitope Generation by Immuno-Proteasomes
  • 3.4. PA28 and Tumor Epitope Processing
  • 3.5. Exploiting Proteasome Knowledge
  • References
  • 4. T Cells In Tumor Immunity
  • 4.1. Introduction
  • 4.2. Morphological Evidence of T Cell Immunity in Human Tumors
  • 4.3. Approaches to the Molecular Identification of Cytolytic T Lymphocyte (CTL)-defined Tumor Antigens
  • 4.4. Monitoring the Spontaneous CTL Responses to Tumor Antigens
  • 4.4.1. Monitoring Specific CTL in the PBMC Compartment
  • 4.4.2. Evidence of Tumor Antigen-specific T Cell Responses at the Tumor Sites
  • 4.5. CD4 T Cells in Tumor Immunity
  • 4.6. Concluding Remarks
  • References
  • Part 2. Immune Evasion and Suppression
  • 5. Major Histocompatibility Complex Modulation and Loss
  • 5.1. The Major Histocompatibility Complex (MHC) Antigen-Processing and -Presentation Pathways
  • 5.1.1. The MHC Class I Antigen-Processing Machinery (APM)
  • 5.1.2. The MHC Class II APM
  • 5.2. The Physiology of the Non-classical HLA-G Molecule
  • 5.3. Determination of the Expression of Classical and Non-classical MHC Antigens
  • 5.4. Interaction between Tumor and the Immune System
  • 5.5. The Different MHC Class I Phenotypes and their Underlying Molecular Mechanisms
  • 5.5.1. MHC Class I Loss
  • 5.5.2. MHC Class I Down-regulation
  • 5.5.3. Selective Loss or Down-regulation
  • 5.6. MHC Class I Alterations: Impact on Immune Responses and Clinical Relevance
  • 5.7. The Role of MHC Class II Processing and Presentation in Tumors
  • 5.7.1. Frequency and Clinical Impact of MHC Class II Expression on Tumors
  • 5.7.2. Molecular Mechanisms of Deficiencies in the MHC class II APM
  • 5.7.3. Modulation of Immune Response by Altered MHC Class II Expression
  • 5.7.4. MHC Class II Expression in Antitumor Response
  • 5.8. Role of IFN-[gamma] in Immunosurveillance
  • 5.8.1. IFN-[gamma]-dependent Immunosurveillance of Tumor Growth
  • 5.8.2. Deficiencies in the IFN Signal Transduction Pathway
  • 5.9. HLA-G Expression: an Immune Privilege for Malignant Cells?
  • 5.9.1. HLA-G Expression in Tumor Cells of Distinct Origin
  • 5.9.2. Clinical Impact of HLA-G Expression
  • 5.9.3. Induction of Tolerance by HLA-G Expression
  • 5.10. Conclusions
  • Acknowledgments
  • References
  • 6. Immune Cells in the Tumor Microenvironment
  • 6.1. Introduction
  • 6.2. The Immune System and Tumor Progression
  • 6.3. Immune Cells in the Tumor Microenvironment
  • 6.4. Phenotypic and Functional Characteristics of Immune Cells Present at the Tumor Site
  • 6.4.1. T Cells
  • 6.4.2. Natural Killer (NK) Cells
  • 6.4.3. DCs
  • 6.4.4. Macrophages
  • 6.4.5. B Cells
  • 6.5. Mechanisms Linked to Dysfunction of Immune Cells in Cancer
  • 6.5.1. The CD95-CD95 Ligand (CD95L) Pathway
  • 6.5.2. T Lymphocyte Apoptosis in Patients with Cancer
  • 6.5.3. Tumor Sensitivity to FasL-Mediated Signals
  • 6.5.4. A Dual Biologic Role of FasL
  • 6.5.5. Contributions of other Pathways to Lymphocyte Demise in Cancer
  • 6.6. Conclusions
  • References
  • 7. Immunosuppressive Factors in Cancer
  • 7.1. Introduction
  • 7.1. Transforming Growth Factor (TGF)-[beta]
  • 7.1.1. Sources of TGF-[beta]
  • 7.1.2. Effects of TGF-[beta]
  • 7.1.2.1. Effects of TGF-[beta] on monocytes/macrophages
  • 7.1.2.2. Effects of TGF-[beta] on T lymphocytes
  • 7.1.2.3. Effects of TGF-[beta] on NK and lymphokine-activated killer (LAK) activity
  • 7.1.2.4. Effects of TGF-1;b on dendritic cells (DCs)
  • 7.1.3. Inhibition of TGF-[beta]: Implications for Therapy
  • 7.2. IL-10
  • 7.2.1. Sources of IL-10
  • 7.2.2. Effects of IL-10
  • 7.2.2.1. Effects of IL-10 on monocytes/macrophages
  • 7.2.2.2. Effects of IL-10 on T lymphocytes
  • 7.2.2.3. Effects of IL-10 on NK cells
  • 7.2.2.4. Effects of IL-10 on DCs
  • 7.2.3. Inhibition of IL-10: Implications for Therapy
  • 7.2.3.1. Antibodies
  • 7.2.3.2. Drugs
  • 7.2.3.3. Removal of the source of IL-10
  • 7.3. Macrophage Migration Inhibitory Factor (MIF)
  • 7.4. Prostaglandin (PG) E[subscript 2]
  • 7.4.1. Sources of PGE[subscript 2]
  • 7.4.2. Effects of PGE[subscript 2]
  • 7.4.2.1. Effects of PGE[subscript 2] on monocytes/macrophages
  • 7.4.2.2. Effects of PGE[subscript 2] on T lymphocytes
  • 7.4.2.3. Effects of PGE[subscript 2] on NK cells and LAK activity
  • 7.4.3. Inhibition of PGE[subscript 2]: Implications for Therapy
  • 7.5. Polyamines
  • 7.5.1. Sources of Polyamines
  • 7.5.2. Effects of Polyamines
  • 7.5.2.1. Effects of polyamines on monocytes/macrophages
  • 7.5.2.2. Effects of polyamines on T lymphocytes
  • 7.5.2.3. Effects of polyamines on NK cells
  • 7.5.3. Inhibition of Polyamine Biosynthesis: Implications for Therapy
  • 7.6. Tumor-Shed Immunosuppressive Molecules
  • 7.7. Conclusion
  • References
  • 8. Interleukin-10 in Cancer Immunity
  • 8.1. Introduction
  • 8.2. IL-10 Protein and IL-10 Receptor (IL-10R)
  • 8.2.1. IL-10 Structure and Expression
  • 8.2.2. IL-10R
  • 8.2.3. IL-10 Homologs
  • 8.3. Biological Activities of IL-10
  • 8.3.1. Effects on Myeloid Antigen-Presenting Cells (APC)
  • 8.3.2. Effects on T Cells
  • 8.3.3. Effects on Natural Killer (NK) Cells
  • 8.3.4. Effects on other Immune Cells
  • 8.3.5. IL-10's Role in the Immune System
  • 8.4. IL-10 Expression in Cancer Patients
  • 8.4.1. Cellular Sources of IL-10 in Cancer Patients
  • 8.4.2. Selectivity of IL-10 Production
  • 8.4.3. IL-10 Presence: Local or Systemic?
  • 8.4.4. Prognostic Value of Enhanced IL-10 Expression
  • 8.5. Effects of IL-10 in Cancer Models
  • 8.5.1. Tumor-Promoting Effects of IL-10
  • 8.5.2. Tumor-Inhibiting Effects of IL-10
  • 8.6. Conclusions
  • Acknowledgements
  • References
  • Part 3. Strategies for Cancer Immunology
  • 9. Dendritic Cells and Cancer: Prospects for Cancer Vaccination
  • 9.1. Introduction
  • 9.2. DC Properties
  • 9.3. DC in Human Cancer
  • 9.4. Blood DC Counts and DC Mobilization
  • 9.5. DC Preparations for Immunotherapy
  • 9.6. Loading DC with Antigens
  • 9.7. Dose Delivery and Vaccination Schedule
  • 9.8. Phase I/II Clinical Trials
  • 9.9. Phase III Clinical Trials
  • 9.10. Side Effects
  • 9.11. Monitoring Immune Responses
  • 9.12. Tumor Escape
  • 9.13. New Developments in DC Immunotherapy
  • 9.14. Conclusion
  • References
  • 10. The Immune System in Cancer: If It Isn't Broken, Can We Fix It?
  • 10.1. Commitment and the Modern Immune System
  • 10.2. Evolutionary Tuning
  • 10.3. Tumor Antigens and Responses to Them
  • 10.4. Antigen Presentation--A Resume
  • 10.5. Playing to Strengths
  • 10.6. Exploiting Weaknesses: Autoimmunity
  • 10.7. Combining the Best of Both Worlds
  • 10.8. The Way Forward
  • Acknowledgments
  • Appendix. Glossary
  • References
  • 11. Hybrid Cell Vaccination for Cancer Immune Therapy
  • 11.1. Introduction
  • 11.2. Immunological Basis of the HCV Approach to Cancer Immune Therapy
  • 11.2.1. Tumor Antigenicity
  • 11.2.2. T-T Cell Collaboration in the Induction of Cellular Cytotoxic Immune Responses
  • 11.3. Vaccination Strategies for Cancer Immune Therapy
  • 11.4. HCV
  • 11.4.1. Conceptual Basis
  • 11.4.2. HCV in Preclinical Studies
  • 11.4.3. Clinical Experience with HCV
  • 11.5. Conclusion and Prospects
  • References
  • 12. Principles and Strategies Employing Heat Shock Proteins for Immunotherapy of Cancers
  • 12.1. The Thesis
  • 12.1.1. HSPs per se are rarely Tumor Antigens
  • 12.1.2. HSPs are Molecular Chaperones for Antigenic Peptides
  • 12.1.3. HSPs are Adjuvants
  • 12.1.4. HSPs are Involved in Cross-Priming
  • 12.1.5. Other Roles
  • 12.2. Cancer Immunotherapy Strategies with HSPs
  • 12.2.1. Strategy 1: Autologous HSPs as Tumor-Specific Vaccines
  • 12.2.2. Strategy 2: HSPs as Adjuvant
  • 12.2.2.1. Non-covalent complex between HSP and antigenic peptides
  • 12.2.2.2. Covalent complex between HSP and antigenic peptides
  • 12.2.3. Strategy 3: Whole Cell Vaccine based on the Modulation of the Expression of HSPs
  • 12.2.3.1. Modulation of the level of HSPs for cancer immunotherapy
  • 12.2.3.2. Modulation of the site of HSP expression for cancer immunotherapy
  • 12.3. Conclusion and Perspectives
  • References
  • 13. Applications of CpG Motifs from Bacterial DNA in Cancer Immunotherapy
  • 13.1. History of Cancer Immunotherapy with Bacterial Extracts and Nucleic Acids
  • 13.2. CpG Motifs in bDNA Explain its Immune Stimulatory Activity
  • 13.3. Identification of a Specific Receptor for CpG motifs, Toll-like Receptor (TLR)-9
  • 13.4. Backbone-dependent Immune Effects of CpG Motifs and Delineation of CpG-A versus CpG-B Classes of ODN
  • 13.5. Applications of CpG DNA in Immunotherapy of Cancer
  • 13.5.1. CpG-A or CpG-B DNA as a Monotherapy
  • 13.5.2. CpG DNA as an Adjuvant for Cancer Vaccines
  • 13.5.3. Application of CpG DNA to Enhance ADCC for Treating Cancer
  • 13.6. Conclusion
  • Acknowledgments
  • References
  • 14. The T-Body Approach: Towards Cancer Immuno-Gene Therapy
  • 14.1. Background
  • 14.2. CRs with Antitumor Specificity
  • 14.2.1. Optimizing the CR Design
  • 14.2.1.1. The single-chain CR
  • 14.2.1.2. Direct recruitment of intracellular triggering molecules
  • 14.2.1.3. Combining stimulatory and co-stimulatory signals
  • 14.2.2. Anticancer Specificaties of CRs
  • 14.2.2.1. Cancer-specific antibodies
  • 14.2.2.2. Ligands and receptors recognition units
  • 14.2.3. Pre-Clinical Experimental Models
  • 14.2.4. Clinical Trials
  • 14.3. Conclusions and Perspectives
  • Acknowledgments
  • References
  • 15. Bone Marrow Transplantation for Immune Therapy
  • 15.1. Introduction
  • 15.2. Graft-versus-Host (GvH) Reactions
  • 15.3. Graft-versus-Tumor (GvT) Effect
  • 15.4. Donor Lymphocyte Infusions (DLIs)
  • 15.5. Complications of DLI: GvHD and Marrow Aplasia
  • 15.6. Strategies to reduce GvHD while preserving GvT
  • 15.7. The Suicide Gene Strategy
  • 15.8. HSV-tk Lymphocyte Add-backs after Haploidentical Transplantation
  • 15.9. Reduced Intensity versus Conventional Conditioning Regimens
  • References
  • 16. Immunocytokines: Versatile Molecules for Biotherapy of Malignant Disease
  • 16.1. Introduction
  • 16.1.1. Immunocytokines
  • 16.1.2. Construction of Immunocytokines
  • 16.1.3. Binding and Cytokine Activity of IL-2 Immunocytokines
  • 16.2. Treatment of Tumor Metastases with Immunocytokines
  • 16.2.1. Colorectal Carcinoma
  • 16.2.2. Long-lived Tumor-Protective Immunity is Boosted by Non-curative Doses of huKS1/4-IL-2 Immunocytokine
  • 16.2.3. Carcinoembryonic Antigen (CEA)-based DNA Vaccines for Colon Carcinoma Boosted by IL-2 Immunocytokine
  • 16.2.4. T Cell-mediated Protective Immunity against Colon Carcinoma Induced by a DNA Vaccine encoding CEA and CD40 Ligand Trimer (CD40LT)
  • 16.3. Non-small Cell Lung Carcinoma
  • 16.3.1. Boost of a CEA-based DNA Vaccine by the huKS1/4-IL-2 Immunocytokine
  • 16.4. Prostate Carcinoma
  • 16.4.1. Suppression of Human Prostate Cancer Metastases by an IL-2 Immunocytokine
  • 16.5. Melanoma
  • 16.5.1. Treatment of Tumor Metastases with Immunocytokines
  • 16.5.2. Tumor Targeting of LT-[alpha] Induces a Peripheral Lymphoid-like Tissue Leading to an Efficient Immune Response against Melanoma
  • 16.5.3. ch14.18-IL-2 Immunocytokine Boosts Protective Immunity Induced by an Autologous Oral DNA Vaccine against Murine Melanoma
  • 16.6. Neuroblastoma
  • 16.6.1. Treatment with ch14.18-IL-2 Immunocytokine
  • 16.6.2. Immunocytokine Treatment of Bone Marrow and Liver Metastases
  • 16.6.3. Mechanism of Immunocytokine-mediated Immune Responses
  • 16.6.4. Amplification of Suboptimal CD8[superscript +] T Memory Cells by a Cellular Vaccine
  • 16.6.5. Synergy between Targeted IL-2 and Antiangiogensis
  • 16.7. Conclusions and Perspectives
  • Acknowledgments
  • References
  • 17. Immunotoxins and Recombinant Immunotoxins in Cancer Therapy
  • 17.1. Introduction
  • 17.2. First- and Second-Generation Immunotoxins
  • 17.3. The Development of Recombinant DNA-based Immunotoxins: Design of Recombinant Immunotoxins
  • 17.3.1. The Toxin Moiety
  • 17.3.1.1. Plant toxins
  • 17.3.1.2. Bacterial toxins: DT and DT derivatives
  • 17.3.1.3. Bacterial toxins: PE and PE derivatives
  • 17.3.2. The Targeting Moiety--Recombinant Antibody Fragments
  • 17.4. Construction and Production of Recombinant Immunotoxins
  • 17.5. Preclinical Development of Recombinant Immunotoxins
  • 17.6. Application of Recombinant Immunotoxins
  • 17.6.1. Recombinant Immunotoxins against Solid Tumors
  • 17.6.2. Recombinant Immunotoxins against Leukemias and Lymphomas
  • 17.7. Isolation of New and Improved Antibody Fragments as Targeting Moieties: Display Technologies for the Improvement of Immunotoxin Activity
  • 17.8. Improving the Therapeutic Window of Recombinant Immunotoxins: The Balance of Toxicity, Immunogenicity and Efficacy
  • 17.8.1. Immune Responses and Dose-limiting Toxicity
  • 17.8.2. Specificity Dictated by the Targeting Moiety
  • 17.9. Conclusions and Perspectives
  • References
  • Glossary
  • Index
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