Tumor Suppressing Viruses, Genes, and Drugs

Innovative Cancer Therapy Approaches

Specificaties
Gebonden, blz. | Engels
Elsevier Science | e druk, 2001
ISBN13: 9780124762497
Rubricering
Elsevier Science e druk, 2001 9780124762497
Verwachte levertijd ongeveer 9 werkdagen

Samenvatting

Tumor Suppressing Viruses, Genes, and Drugs profiles the new generation of cancer treatments now in development. The book examines the innovative new approaches of viral, gene, and signal therapies that promise to replace or enhance conventional methods such as surgery, radiation, and chemotherapy. The timely information presented by this book should be of interest to anyone concerned with advancing cancer treatment beyond current medical practices.

Specificaties

ISBN13:9780124762497
Taal:Engels
Bindwijze:Gebonden

Inhoudsopgave

<br>Contributors</br><br>Preface</br><br>1 Oncolytic Viruses: Virotherapy for Cancer</br><br> I. Introduction</br><br> II. Attributes of Replication-Selective Viruses for Cancer Treatment</br><br> III. Approaches to Optimizing Tumor-Selective Viral Replication</br><br> IV. Adenoviruses</br><br> V. Poliovirus</br><br> VI. Vesicular Stomatitis Virus</br><br> VII. Reovirus</br><br> VIII. Bacteria</br><br> IX. Vaccinia Virus</br><br> X. Herpesvirus</br><br> XI. Clinical Trial Results with Replication-Competent Adenoviruses in Cancer Patients</br><br> XII. Results from Clinical Trials with dl1520 (Onyx-015, or CI-1042)</br><br> XIII. Future Directions: Approaches to Improving the Efficacy of Replication-Selective Viral Agents</br><br> XIV. Summary</br><br> References</br><br>2 Reovirus Therapy of Ras-Associated Cancers</br><br> I. Introduction</br><br> II. Reovirus Oncolysis</br><br> III. Concluding Remarks</br><br> References</br><br>3 Oncolytic Herpes Simplex Virus (G207) Therapy: From Basic to Clinical</br><br> I. Introduction</br><br> II. Preclinical Studies of G207</br><br> III. G207 Clinical Trial</br><br> IV. Conclusions</br><br> References</br><br>4 p53 and Its Targets</br><br> I. Introduction</br><br> II. Activation of p53</br><br> III. Downstream Mediators of p53</br><br> References</br><br>5 Prospects for Tumor Suppressor Gene Therapy: RB as an Example</br><br> I. Introduction</br><br> II. Functions of RB</br><br> III. Successes with RB Gene Therapy </br><br> IV. Perspectives</br><br> References</br><br>6 CDK Inhibitors: Genes and Drugs</br><br> I. Introduction</br><br> II. G1 Regulation </br><br> III. p16INK4a and the Rb Pathway</br><br> IV. p19ARF and p53 Pathway</br><br> V. p27 and Human Cancer</br><br> VI. Conclusions and Future Perspectives</br><br> References</br><br>7 CDK Inhibitors: Small Molecular Weight Compounds</br><br> I. Introduction</br><br> II. Cyclin-Dependent Kinases, the Cell Cycle, and Cancer</br><br> III. Cyclin-Dependent Kinase Inhibitors, a Large Variety of Structures</br><br> IV. Cyclin-Dependent Kinase Inhibitors, All Competing with ATP</br><br> V. Cyclin-Dependent Kinase Inhibitors, the Selectivity Problem</br><br> VI. Cyclin-Dependent Kinase Inhibitors, Cellular Effects</br><br> VII. Cyclin-Dependent Kinase Inhibitors, Antitumor Activity</br><br> VIII. Conclusion</br><br> References</br><br>8 NF1 and Other RAS-Binding Peptides</br><br> I. RAS Molecules: Normal versus Oncogenic Mutants </br><br> II. Super GAP?</br><br> III. RAS-Binding Fragment of NF1</br><br> IV. c-RAF-1</br><br> V. PI-3 Kinase</br><br> VI. Ral GDS </br><br> References</br><br>9 Cytoskeletal Tumor Suppressor Genes</br><br> I. Introduction (Historical Background)</br><br> II. Type I Cytoskeletal Tumor Suppressors</br><br> III. Type II Cytoskeletal Tumor Suppressors</br><br> References</br><br>10 TGF-? Signaling and Carcinogenesis</br><br> I. Introduction</br><br> II. Dual Role of TGF-? in Carcinogenesis</br><br> III. TGF-? Superfamily Signaling</br><br> IV. Perturbation of TGF-? Signaling in Cancer Cells</br><br> V. Perspectives</br><br> References</br><br>11 DAN Gene</br><br> I. Introduction</br><br> II. Cloning of DAN cDNA</br><br> III. Transfection of DAN</br><br> IV. Role of DAN in Neuroblastomas</br><br> V. Structural Features of the DAN Protein</br><br> VI. Genomic Structure of DAN</br><br> VII. DAN Family</br><br> References</br><br>12 Design of Hammerhead Ribozymes and Allosterically Controllable Maxizymes for Cancer Gene Therapy</br><br> I. Introduction</br><br> II. Ribozyme Expression System in Cells</br><br> III. Design of the tRNAVal-Driven Ribozyme That Is Transcribed by pol III</br><br> IV. Design of Allosterically Controlled Maxizymes</br><br> V. Conclusion</br><br> References</br><br>13 Inhibitors of Angiogenesis</br><br> I. Introduction—Angiogenesis</br><br> II. Angiogenesis Inhibitors</br><br> III. Future Directions</br><br> References</br><br>14 Geranylgeranylated RhoB Mediates the Apoptotic and Antineoplastic Effects of Farnesyltransferase Inhibitors: New Insights into Cancer Cell Suicide</br><br> I. Introduction </br><br> II. Do Farnesyltransferase Inhibitors Target a Unique Aspect of Neoplastic Pathophysiology?</br><br> III. Ras Is Not a Crucial Target of Farnesyltransferase Inhibitors</br><br> IV. RhoB Is a Crucial Target of Farnesyltransferase Inhibitors</br><br> V. Farnesyltransferase Inhibitors Act through a Gain of Function Mechanism Involving RhoB-GG</br><br> VI. RhoB-GG Is Required to Mediate Apoptosis by Farnesyltransferase Inhibitors</br><br> VII. RhoB-GG and the Antiangiogenic Properties of Farnesyltransferase Inhibitors</br><br> VIII. Clinical Implications</br><br> IX. Summary</br><br> References</br><br>15 RAS Binding Compounds</br><br> I. Introduction</br><br> II. Ras Cycle and Ras–Raf Signaling Pathway</br><br> III. The Structure of Ras Proteins</br><br> IV. Drug Target Sites of Ras</br><br> V. Conclusions and Outlook</br><br> References</br><br>16 Actin-Binding Drugs: MKT-077 and Chaetoglobosin K (CK)</br><br> I. Introduction</br><br> II. MKT-077: F-Actin Bundler</br><br> III. Chaetoglobosin K: F-Actin Capper</br><br> References</br><br>17 Tyr Kinase Inhibitors as Potential Anticancer Agents: EGF Receptor and ABL Kinases</br><br> I. Introduction</br><br> II. Tyr Kinase Inhibitors</br><br> III. Chronic Myelogenous Leukemia</br><br> IV. Epidermal Growth Factor Receptor</br><br> V. Antagonists of the Epidermal Growth Factor Receptor Extracellular Domain</br><br> VI. Chemical Inhibitors of the Kinase Domain of the Epidermal Growth Factor Receptor</br><br> VII. Epidermal Growth Factor Receptor Antagonists or Inhibitors Act Synergistically to Kill Tumor Cells</br><br> VIII. The Effects of Abl Inhibitors on Leukemia</br><br> References</br><br>18 Antagonists of Rho Family GTPases: Blocking PAKs, ACKs, and Rock</br><br> I. Rho Family GTPases (Rho, Rac, and CDC42)</br><br> II. Blocking PAKs</br><br> III. Blocking CDC42 Pathways (ACKs and N-WASP)</br><br> IV. Blocking Rho Pathways</br><br> V. Rac-Specific Inhibitors?</br><br> References</br><br>19 Integrin Antagonists as Cancer Therapeutics</br><br> I. Introduction</br><br> II. Signaling Pathways Activated by Integrins</br><br> InII. Role of Integrins in Neoplastic Transformatio</br><br> IV. Role of Integrins in Tumor-Induced Angiogenesis</br><br> V. Integrin Antagonists as Antiangiogenesis Agents</br><br> VI. Conclusions and Future Perspectives</br><br> References</br><br>20 Functional Rescue of Mutant p53 as a Strategy to Combat Cancer</br><br> I. Introduction </br><br> II. Multiple Pathways of p53-Induced Apoptosis</br><br> III. Regulation of p53 Activity</br><br> IV. Approaches toward Reactivation of Mutant p53</br><br> V. Implications for Tumor Therapy and Future Perspectives</br><br> References</br><br>Index</br>

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        Tumor Suppressing Viruses, Genes, and Drugs