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Anticancer Genes

Tác giả: Grimm, Stefan

Chủ đề:

Chủ đề: Medicine; Cancer; Anticancer Genes

Nhà xuất bản: Springer

Năm xuất bản: 2014

Loại tài liệu: Book

Mô tả vật lý: 287 p.

Định danh: 978-1-4471-6458-6

Ngôn ngữ: en

Liên kết: Advances in Experimental Medicine and Biology;Book 818

Đọc trực tuyến

Tải tài liệu

Anticancer Genes provides an overview of this nascent field, its genesis, current state, and prospect. It discusses how Anticancer Genes might lead to the identification of a repertoire of signaling pathways directed against cellular alterations that are specific for tumor cells.

Cover
Advances in Experimental Medicine and Biology
Title pages
Contents
Contributors
Chapter 1: Introduction
- 1.1 The Quest for Novel Agents in Cancer Treatment
- 1.2 Anticancer Genes
- 1.3 Expectations of Anticancer Genes
- 1.4 Synthetic Lethality: The Genetic Basis of Anticancer Genes
- References
Part I: Viral Anticancer Genes
- Chapter 2: Signalling of Apoptin
  - 2.1 Introduction to Apoptin
  - 2.2 Structure of Apoptin
  - 2.3 Cell Type-Specific Localization of Apoptin
  - 2.4 Tumor-Specific Phosphorylation of Apoptin
  - 2.5 Interacting Proteins
    - 2.5.1 Protein Kinase C (PKC)
    - 2.5.2 Bcl-10 and Fas-Associated Protein with Death Domain (FADD)
    - 2.5.3 Protein Kinase G (PKG-I)
    - 2.5.4 PI3-Kinase (PI3K) and Akt
    - 2.5.5 Heat Shock Cognate Protein 70 (Hsc70)
    - 2.5.6 Promyelocytic Leukemia Protein (PML)
    - 2.5.7 Anaphase Promoting Complex 1 (APC1)
    - 2.5.8 Hip-1 Protein Interactor (Hippi)
    - 2.5.9 Death Effector Domain-Associated Factor (DEDAF)
    - 2.5.10 Peptidyl-Prolyl Isomerase-Like 3 (Ppil3)
    - 2.5.11 N-Myc Interacting Protein (Nmi)
    - 2.5.12 Breast Cancer Associated Gene 3 (Bca3)
  - 2.6 Mechanism of Apoptin-Induced Cell Death
    - 2.6.1 Apoptotic Pathways
    - 2.6.2 Induction of Apoptotic Pathways by Apoptin
    - 2.6.3 Role of the Tumor Suppressors p53 and p73
    - 2.6.4 Induction of G2/M Arrest
    - 2.6.5 Mitotic Catastrophe
    - 2.6.6 Ceramide Signalling
    - 2.6.7 Summary
  - 2.7 Conclusive Remarks
  - References
- Chapter 3: Apoptin Towards Safe and Efficient Anticancer Therapies
  - 3.1 Cancer
  - 3.2 Cancer Therapies
  - 3.3 Virus-Derived Vectors
    - 3.3.1 Adenovirus Vectors
    - 3.3.2 Apoptin Enhances Oncolytic Properties of Newcastle Disease Virus and Parvovirus-H1
    - 3.3.3 Alternative Viral Systems
  - 3.4 Plasmid-Based Vectors
  - 3.5 Protein Therapy
  - 3.6 Combinatorial Therapies
  - 3.7 Attenuated Salmonella Typhimurium
  - 3.8 Apoptin-Derivates Act as Targeting Tool
  - 3.9 Sensor of Potential Drug Targets
  - 3.10 Bcr-Abl
  - 3.11 Ceramide
  - 3.12 Proteasomes
  - 3.13 Inactivated Phosphatase 2A Promotes Tumor Formation and Activates Apoptin
  - 3.14 Mitotic Catastrophe
  - 3.15 Conclusions
  - References
- Chapter 4: Induction of Cancer-Specific Cell Death by the Adenovirus E4orf4 Protein
  - 4.1 E4orf4 Induces a Unique Form of Cancer-Specific Cell Death
  - 4.2 E4orf4 in Virus Infection
    - 4.2.1 The Adenovirus Early Region 4 Transcription Unit (E4) and E4 Proteins
    - 4.2.2 E4orf4 Structure
    - 4.2.3 E4orf4 Functions During Viral Infection
    - 4.2.4 Protein Phosphatase 2A Is a Major E4orf4 Partner, Which Contributes to E4orf4 Functions During Adenovirus Infection
    - 4.2.5 Determination of E4orf4 and PP2A-B55 Binding Sites
  - 4.3 E4orf4-Induced Cell Death
    - 4.3.1 Caspase-Independent Cell Death and Crosstalk with Other Forms of Cell Death
    - 4.3.2 Morphological Hallmarks of E4orf4-Induced Cell Death and Assays for Measuring E4orf4-Induced Cell Killing
    - 4.3.3 E4orf4 Cellular Localization: Nuclear vs. Cytoplasmic Cell Death
  - 4.4 E4orf4 and Its Protein Partners
    - 4.4.1 The E4orf4-Src Kinase Interaction and Its Contribution to Induction of Cell Death
    - 4.4.2 The Contribution of the E4orf4-PP2A Interaction to E4orf4-Induced Cell Death
      - 4.4.2.1 Association of E4orf4 with PP2A Phosphatase Activity Correlates with E4orf4-Induced Cell Death
      - 4.4.2.2 How Does PP2A Contribute to E4orf4-Induced Cell Death?
        
        Does E4orf4 Affect PP2A Activity?
        
        E4orf4 Recruits PP2A to Potential Substrates: ACF and APC/C
  - 4.5 The Mechanisms Underlying E4orf4-Induced Toxicity Are Highly Conserved in Evolution
    - 4.5.1 Lessons from the Yeast S. cerevisiae on E4orf4-Induced Toxicity
      - 4.5.1.1 E4orf4-Induced Cell Cycle Arrest Leads to Cell Death in Yeast and Mammalian Cells
      - 4.5.1.2 A Genetic Screen in Yeast Revealed Another Contributor to E4orf4-Induced Toxicity: Ynd1/Golgi UDPase
    - 4.5.2 Lessons from Drosophila melanogaster on E4orf4-Induced Toxicity
  - 4.6 Preliminary Exploration of the Therapeutic Potential of E4orf4
  - 4.7 Future Directions
  - References
- Chapter 5: Tumor Suppressing Properties of Rodent Parvovirus NS1 Proteins and Their Derivatives
  - 5.1 Introduction
  - 5.2 Actions of Parvovirus NS1
    - 5.2.1 Properties and Functions of the Parvoviral NS1 Protein
    - 5.2.2 NS1 Cytotoxicity - Multiple Functions, Different Manifestations, Gazillions of Targets
  - 5.3 Molecular Determinants of Parvovirus NS1
    - 5.3.1 NS1 Domain Structure
    - 5.3.2 Functional Interplay Between Different NS1 Domains
    - 5.3.3 NS1 Regulation - Dependence on the PDK/PKC/PKB Pathway
    - 5.3.4 Differences Among Rodent PV NS1 Proteins
    - 5.3.5 Producing Artificial NS1-Derived Polypeptides with Specific Functions
  - 5.4 Parvovirus NS1 - An Oncolytic Agent for Cancer Therapy
    - 5.4.1 Exploiting NS1 Toxicity Functions in Cancer Therapy
    - 5.4.2 Prospect: Generation of Chimeric Oncotropic Viruses Armed with PV NS1 or NS1-Related-Toxin(s)
  - References
Part II: Cellular Anticancer Genes
- Chapter 6: MDA-7/IL-24: Multifunctional Cancer Killing Cytokine
  - 6.1 Introduction
  - 6.2 MDA-7/IL-24
  - 6.3 Role of MDA-7/IL-24 in Cancer
    - 6.3.1 Apoptosis
    - 6.3.2 Autophagy
    - 6.3.3 Anti-angiogenesis
    - 6.3.4 Inhibition of Invasion and Metastasis
  - 6.4 Combination Effects of MDA-7/IL-24
  - 6.5 Phase I Clinical Trial with Ad.mda-7 (INGN-241)
  - 6.6 Conclusions and Future Prospectives
  - References
- Chapter 7: Cancer-Selective Apoptosis by Tumor Suppressor Par-4
  - 7.1 Introduction
  - 7.2 Apoptosis by Par-4
  - 7.3 The Leucine Zipper Domain
  - 7.4 The SAC Domain
  - 7.5 SAC Transgenic Mice Show Tumor Resistance
  - References
- Chapter 8: Tumor-Necrosis-Factor-Related Apoptosis-Inducing Ligand (TRAIL)
  - 8.1 Introduction
  - 8.2 Apoptosis Signaling Pathways
  - 8.3 The TRAIL Receptor/Ligand System
  - 8.4 Pro- and Antiapoptotic Mechanisms that Control Cancer Cells´ Sensitivity Towards TRAIL
  - 8.5 Strategies to Target the TRAIL Receptor Ligand System for Therapeutic Purposes
    - 8.5.1 TRAIL Receptor Agonists
    - 8.5.2 TRAIL-Based Combined Treatments
    - 8.5.3 Clinical Studies with TRAIL Receptor Agonists
  - 8.6 Conclusions
  - References
- Chapter 9: SIRT6: A Promising Target for Cancer Prevention and Therapy
  - 9.1 Introduction: Understanding Cancer as an Age-Related Disease
  - 9.2 Sirtuins: A Family of Longevity Genes
  - 9.3 SIRT6
  - 9.4 SIRT6 and Cancer
    - 9.4.1 SIRT6 Suppresses Tumor Formation by Regulating Cellular Metabolism
    - 9.4.2 SIRT6 Suppresses Tumor Initiation by Mediating c-FOS Dependent Apoptosis
    - 9.4.3 SIRT6 May Suppress Tumorigenesis by Promoting Genome Stability
    - 9.4.4 SIRT6: A Potential Role in Controlling Tumorigenesis by Suppressing Inflammation
  - 9.5 Therapeutic Activation of SIRT6
  - 9.6 Conclusion
  - References
- Chapter 10: An Overview of Brevinin Superfamily: Structure, Function and Clinical Perspectives
  - 10.1 Introduction
  - 10.2 Gene Organization and cDNA Cloning
  - 10.3 The Recombinant Expression of AMPs
  - 10.4 Anti-pathogen Activity of Brevinins
  - 10.5 Effect of Brevinins on Cytokine Release
  - 10.6 Anticancer Activity of Brevinins
  - 10.7 Other Activities of Brevinins
  - 10.8 Functionalization of Nanostructures with Peptides
  - 10.9 Closing Remarks
  - References
- Chapter 11: Isolation and Characterization of the Anticancer Gene Organic Cation Transporter Like-3 (ORCTL3)
  - 11.1 ORCTL3 - Cloning and Mapping
  - 11.2 Structure and Tissue Distribution
  - 11.3 Physiological Function
  - 11.4 Anticancer Function
  - 11.5 Universal Anticancer Activity?
  - 11.6 Structure and Mechanism of the Anticancer Protein ORCTL3
  - 11.7 In Vivo Applications
  - 11.8 The Future of ORCTL3 as an Anticancer Gene
  - References
Part III: Anticancer Gene Therapy
- Chapter 12: Introduction of Genes via Sonoporation and Electroporation
  - 12.1 Introduction
  - 12.2 Sonoporation-Definition
  - 12.3 Ultrasound Field-Unfocused and Focused
    - 12.3.1 Unfocused Beams
    - 12.3.2 Focused Beams
  - 12.4 Properties of Microbubbles
  - 12.5 Microbubble Interaction Leading to Sonoporation
  - 12.6 Sonoporation Pore Size
  - 12.7 Ultrasound Parameters Affecting Sonoporation and Delivery Efficiency
  - 12.8 Mechanism of Gene Delivery via Sonoporation
  - 12.9 In Vitro Studies of Sonoporation in Cell Cultures
  - 12.10 In Vivo Studies of Sonoporation
  - 12.11 Future Prospects and Development
  - 12.12 Electroporation: Definition
  - 12.13 Pore Formation and Cell Membrane Permeability
  - 12.14 Parameters Affecting Electroporation and Delivery Efficiency
  - 12.15 Electroporation: Instrumentation
  - 12.16 In Vitro Electroporation
  - 12.17 In Vivo Electroporation
  - 12.18 Future Prospects and Development
  - References
- Chapter 13: Anticancer Gene Transfer for Cancer Gene Therapy
  - 13.1 Introduction
    - 13.1.1 Cancer Gene Therapy - Oncolysis
    - 13.1.2 Viral Tropism - Viral Arming
    - 13.1.3 Gene Delivery - Viral and Non-viral Systems
    - 13.1.4 Oncolytic Viruses and Vector Systems for Gene Delivery
    - 13.1.5 Viral Tropism Manipulation
    - 13.1.6 Cancer Specific Proteases and Oncolytic Activation
    - 13.1.7 Cancer Specific Transcription and Replication
    - 13.1.8 Cancer-Specific Promoters
    - 13.1.9 Viral Binding Through Tumor-Specific Receptors
    - 13.1.10 Viral Vectors for Transgene Delivery
    - 13.1.11 Adenoviruses
    - 13.1.12 Adeno-Associated Vectors (AAVs)
    - 13.1.13 Herpes Simplex Viruses
    - 13.1.14 Pox Viruses
    - 13.1.15 Retroviruses-Lentiviruses
    - 13.1.16 Arming Viruses for Cytotoxic Virotherapy
    - 13.1.17 Pro-drug Arming
    - 13.1.18 Microenvironment Gene Manipulation Arming
    - 13.1.19 Pro-apoptotic Genes Arming
    - 13.1.20 Hurdles for the Use of Viruses as Delivery Vectors
  - 13.2 Conclusions-Future of the Field
  - References
Index