Elsevier S & T

Advances in Cancer Research

Vande Woude, George F.; Klein, George

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Table of contents
  • Contentsv
  • Contributors to Volume 97ix
  • Dedicationxiii
  • George Vande Woudexiii
  • Klas Wimanxiv
  • Olle Ringdeacutenxiv
  • Carl-Henrik Heldin and Arne Oumlstmanxiv
  • Alan R. Fershtxv
  • Peter H. Krammerxv
  • Kenneth Nilssonxv
  • Marie Henrikssonxvi
  • Chapter 1: Structural Biology of the Tumor Suppressor p53 and Cancer-Associated Mutants1
  • Abbreviations1
  • I. Introduction2
  • II. The Domain Structure of Human p532
  • III. The Structure of the DNA-Binding Domain4
  • A. p53C Has Evolved to Be Unstable7
  • B. Design of a Superstable Variant of p53C7
  • C. From Core Domain to the Full-Length Protein8
  • IV. Effects of Common Cancer Mutations8
  • A. Structural Effects of Oncogenic Mutations11
  • V. Rescuing Mutant p5315
  • A. Lessons from Second-Site Suppressor Mutations16
  • B. p53C as a Drug Target16
  • VI. Concluding Remarks19
  • References19
  • Chapter 2: Immunotherapy by Allogeneic Stem Cell Transplantation25
  • I. Introduction26
  • II. Graft-Versus-Host Disease27
  • A. Mechanisms27
  • B. Acute GVHD28
  • C. Chronic GVHD29
  • D. Prevention and Treatment of GVHD29
  • III. The Graft-Versus-Leukemia Effect30
  • A. Preliminary Studies30
  • B. Tumor Burden31
  • C. Enhancement of Graft-Versus-Leukemia31
  • D. Cytotoxic T Cells33
  • E. Pathophysiology of Graft-Versus-Leukemia34
  • IV. NK Cells34
  • V. Early Detection of Relapse35
  • A. Minimal Residual Disease35
  • B. Mixed Chimerism35
  • C. Molecular Detection of CML36
  • D. Immunoglobulin and T Cell Receptor Gene Rearrangement36
  • VI. The Graft-Versus-Cancer Effect37
  • A. Immunotherapy Against Cancer37
  • B. Reduced Intensity Conditioning and Allogeneic Stem Cell Transplantation38
  • C. Reduced Intensity Conditioning and Stem Cell Transplantation for Renal Carcinoma38
  • D. Reduced Intensity Conditioning and Stem Cell Transplantation for Various Solid Tumors39
  • E. Combined Liver Transplantation and Stem Cell Transplantation for Liver Cancer40
  • F. Future of Stem Cell Transplantation for Solid Cancers41
  • VII. Mesenchymal Stem Cells41
  • A. Surface Markers and Homing41
  • B. Immunity and Safety of MSCs42
  • C. Immunomodulation by MSC42
  • D. Immunosuppressive Mechanisms by MSCs43
  • VIII. Future Directions44
  • Acknowledgments47
  • References47
  • Chapter 3: Mnt Takes Control as Key Regulator of the Myc/Max/Mxd Network61
  • I. Myc: The Most Frequently Deregulated Oncogene in Human Tumors62
  • A. Myc in Control of Cell Fate62
  • B. Deregulation of Myc in Tumor Development64
  • C. Myc as a Therapeutic Target for Human Cancer65
  • II. Mnt: The Key Transcriptional Regulator of the Myc/Max/Mxd Network66
  • A. Discovery and Characterization of Mnt66
  • B. Mnt, the Major Myc Antagonist67
  • C. Effects of Mnt Deficiency68
  • D. Relief of Mnt-Mediated Repression: The Critical Event for Myc Target Gene Activation69
  • E. Mnt to Be or Not to Be a Tumor Suppressor73
  • III. Concluding Remarks75
  • Acknowledgments75
  • References76
  • Chapter 4: Lytic Cycle Switches of Oncogenic Human Gammaherpesviruses81
  • I. Two Life Cycles of EBV and KSHV: Latency and Lytic Replication82
  • II. Virally Encoded Lytic Cycle Activator Genes84
  • A. Upstream and Downstream Events in Lytic Cycle Activation85
  • B. Agents That Induce the Lytic Cycle89
  • C. Role of Phosphorylation in the Downstream Functions of the EBV ZEBRA Protein97
  • III. Conclusions: Some Unsolved Mysteries About Lytic Cycle Switches of Oncogenic Human Gammaherpesv103
  • Acknowledgments105
  • References105
  • Chapter 5: No Life Without Death111
  • I. Introduction111
  • II. Apoptosis in Life and Disease112
  • III. The Apoptotic Machinery113
  • A. Mitochondria and Cell Death: The Intrinsic Pathway113
  • B. DR-Induced Apoptosis: The Extrinsic Pathway115
  • IV. The CD95/CD95L System116
  • A. Regulation of CD95L Expression in Activation-Induced Cell Death118
  • B. Transcriptional Regulation of CD95L Expression in T Cells120
  • C. Regulation of CD95L Expression by Oxidative Signals123
  • V. HIV and Apoptosis126
  • A. The Genetic Structure of HIV127
  • B. HIV Proteins and Apoptosis127
  • Acknowledgments129
  • References129
  • Chapter 6: Control of Apoptosis in Human Multiple Myeloma by Insulin-like Growth Factor I (IGF-I)139
  • I. Selected Biological Properties of Human Multiple Myeloma140
  • II. Human MM Models In Vitro and In Vivo142
  • III. Targeting Anti-apoptosis and Proliferative Signals in Human MM143
  • A. Anti-apoptotic Events in Human MM143
  • B. The IGF-I Signaling Pathways146
  • C. IGF-I as a Growth and Survival Factor in MM148
  • D. IGF-I as a Target for Therapy149
  • IV. The Effect of Combinational Treatment with PPP on Human MM Cells Is Additive and Synergistic154
  • Acknowledgments159
  • References159
  • Chapter 7: c-MYC Impairs Immunogenicity of Human B Cells167
  • I. Introduction168
  • II. Personal Perspective by G.W.B.168
  • III. Taking Over the Work from Eva and George...172
  • A. Growth Pattern and Cell Surface Phenotype of Burkitt's Lymphoma Cells Can Be Recapitulated by c-m172
  • B. Conditional B Cells Driven into Proliferation by c-myc Overexpression Loose Their Ability to Stim174
  • C. c-MYC Down-Regulates NF-kappaB and Interferon Response Genes177
  • D. c-MYC Impairs the Interferon Response at Different Levels: At the Level of Induction as Well as a180
  • IV. Discussions180
  • Acknowledgments183
  • References184
  • Chapter 8: Cancer Dormancy: Lessons from a B Cell Lymphoma and Adenocarcinoma of the Prostate189
  • I. Introduction190
  • II. Scope of the Present Discussion190
  • III. Clinical Studies192
  • IV. Experimental Dormancy of B Cell Lymphoma193
  • V. The Prostate Adenocarcinoma Model195
  • VI. Concluding Remarks197
  • Acknowledgments198
  • References198
  • Chapter 9: Therapeutic Targets of Multiple Angiogenic Factors for the Treatment of Cancer and Metast203
  • I. Introduction204
  • II. Tumor Angiogenesis205
  • A. Tumor Blood Vessels205
  • B. Tumor-Produced Angiogenic Factors206
  • C. VEGF Family and VEGF Receptors207
  • D. VEGF-A-Induced Angiogenesis and Permeability208
  • E. Non-VEGF Angiogenic Factors210
  • III. Angiogenesis Inhibitors210
  • A. Growth Factor Antagonists211
  • B. VEGF-A Antagonists211
  • C. Antagonists for Non-VEGF Factors212
  • D. Broad-Spectrum Endogenous Inhibitors212
  • E. Oral Angiogenesis Inhibitors213
  • IV. Lymphangiogenesis and Lymphatic Metastasis215
  • V. Clinical Development of Antiangiogenic Drugs216
  • VI. Conclusions and Perspectives217
  • Acknowledgments218
  • References219
  • Chapter 10: Novel Three-Dimensional Organotypic Liver Bioreactor to Directly Visualize Early Events225
  • I. Introduction226
  • A. Metastasis226
  • B. Models to Study Metastasis228
  • II. Bioreactors230
  • A. Liver Bioreactor232
  • III. Tumor Growth in the Bioreactor233
  • IV. Tumor-Hepatocyte Juxtapositioning236
  • V. Future Studies239
  • Acknowledgments241
  • References242
  • Chapter 11: PDGF Receptors as Targets in Tumor Treatment247
  • I. Molecular Biology of PDGF248
  • A. PDGF Isoforms and PDGF Receptors249
  • B. Signaling via PDGF Receptors249
  • II. Physiological Roles of PDGF251
  • III. Roles of PDGF Receptors in Tumors252
  • A. PDGF Stimulation of Malignant Cells252
  • B. Tumor Angiogenesis and PDGF Receptor Signaling257
  • C. PDGF and Recruitment of Tumor Fibroblasts259
  • D. Regulation of Tumor Drug Uptake and IFP by PDGF Receptors260
  • E. Implications of Roles for PDGF Receptor Signaling in Metastasis261
  • IV. Clinical Studies263
  • A. PDGF Antagonists263
  • B. Clinical Effects Ascribed to PDGF Receptor Inhibition264
  • V. Future Perspectives266
  • Acknowledgments267
  • References267
  • Chapter 12: Extracellular Matrix, Nuclear and Chromatin Structure, and Gene Expression in Normal Tis275
  • I. Introduction276
  • II. The ECM277
  • III. ECM-Response DNA Elements278
  • IV. Potential Mechanisms for the Transcriptional Activation of ECM-Response DNA Elements280
  • A. Exposure to ECM Influences the Nuclear Translocation and DNA-Binding Properties of SpecificTransc280
  • B. Exposure to ECM May Initiate Mechanical Signals That Alter the Organization of Nuclear Factors in281
  • C. ECM-Induced Activation of DNA-Response Elements Involves Mechanisms That Invoke Changes in Chroma282
  • V. Potential Mechanisms Through Which ECM Influences the General Organization of Nuclear Factors and284
  • A. Of Mouse and Women: Application to Human Breast Epithelial Cells284
  • B. ECM-Induced Differentiation May Involve the Selective Activation of Particular Tissue-Specific Ge285
  • C. ECM-Induced Changes in Overall Chromatin Structure May Have Profound Implications on Nuclear Orga286
  • VI. Advancing Toward a Deeper Understanding of the Malignant Phenotype287
  • VII. A 3D Reconstruction for the Future of Cancer Research289
  • Acknowledgments289
  • References289
  • Chapter 13: Targeted Cancer Therapy: Promise and Reality295
  • I. What Is Signal Transduction Therapy?295
  • II. Types of Signaling Inhibitors296
  • A. Protein Kinases297
  • B. Targeting Cellular Proliferation297
  • C. Targeting Cell Survival298
  • D. Targeting Angiogenesis298
  • E. Targeting Nuclear Factors298
  • III. Signaling Networks299
  • IV. Target and Drug Evaluation Using Preclinical Tumor Models300
  • A. In Vitro Screens300
  • B. In Vivo Models: Xenografts301
  • C. Transgenic Models302
  • D. Clinical Trials303
  • V. How Successful Is Signal Transduction Therapy in the Clinic?303
  • A. CML and Gleevec304
  • B. Inhibiting the EGFR Family307
  • VI. Using PK Receptors as Homing Molecules for Cancer Therapy310
  • VII. Conclusions311
  • References312
  • Chapter 14: Restoration of Wild-Type p53 Function in Human Tumors: Strategies for Efficient Cancer T321
  • I. The Emergence of p53 as a Key Tumor Suppressor321
  • II. P53 Biological Activity and Binding to DNA322
  • A. p53 Responds to Cellular Stress and Induces Cell Cycle Arrest and Apoptosis322
  • B. p53 DNA Binding and Regulation of Transcription of Downstream Target Genes324
  • III. Reactivation of Mutant p53326
  • A. A Mutant p53-Targeting Peptide326
  • B. Second-Site Mutations326
  • C. Screening for Mutant p53-Targeting Small Molecules327
  • IV. Virus-Based Therapeutic Strategies for Mutant p53-Carrying Tumors330
  • A. Adp53 Gene Therapy330
  • B. ONYX-015: A Replication-Deficient Adenovirus330
  • V. Concluding Remarks331
  • Acknowledgments333
  • References333
  • Index339
Book details
  • Vendor Elsevier S & T
  • SKU 9780120066971
  • ISBN-13 9780080488202
  • Author Vande Woude, George F.; Klein, George
  • Category Medical
  • Subject Oncology

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The Advances in Cancer Research series provides invaluable information on the exciting and fast-moving field of cancer research. A very special event the Nobel Minisymposium, “Molecular Oncology – From Bench to Bedside,” held at the Karolinska Instituet, in Stockholm, Sweden, was marked the celebration of George and Eva Klein’s combined 160th birthday. To honor this occasion, this volume brings together contributions by their former students, colleagues and collaborators of the past fifty years into a volume of Advances in Cancer Research dedicated to George and Eva. Over a decade ago, a subdivision of ACR called “Foundations in Cancer Research” was initiated and the tributes honoring the Kleins’ bodies of work presented at the minisymposium are especially appropriate for the series.