Advances in Cancer Research

 
 
Academic Press
  • 1. Auflage
  • |
  • erschienen am 31. März 2016
  • |
  • 312 Seiten
 
E-Book | ePUB mit Adobe DRM | Systemvoraussetzungen
978-0-12-805181-8 (ISBN)
 

Advances in Cancer Research provides invaluable information on the exciting and fast-moving field of cancer research, presenting outstanding and original reviews on a variety of topics.

 

  • Provides information on cancer research
  • Outstanding and original reviews
  • Suitable for researchers and students
0065-230X
  • Englisch
  • San Diego
  • |
  • USA
Elsevier Science
  • 9,73 MB
978-0-12-805181-8 (9780128051818)
0128051817 (0128051817)
weitere Ausgaben werden ermittelt
  • Front Cover
  • Advances in Cancer Research
  • Copyright
  • Contents
  • Contributors
  • Chapter One: The Evolving, Multifaceted Roles of Autophagy in Cancer
  • 1. Introduction
  • 2. Overview of Autophagy
  • 2.1. Molecular Machinery of Autophagosome Biogenesis
  • 2.1.1. Initiation of Autophagosome Biogenesis by the ULK Complex
  • 2.1.2. Nucleation of the Phagophore by the Class III PI3K Complex
  • 2.1.3. Elongation of the Phagophore by the mAtg12 and LC3 Conjugation Systems
  • 2.2. Fusion
  • 2.3. Regulation of Mammalian Autophagy
  • 2.3.1. Nutrient and Growth Factor Starvation
  • 2.3.2. Hypoxia
  • 2.3.3. Oxidative Stress
  • 2.3.4. Endoplasmic Reticulum Stress
  • 2.3.5. DNA Damage
  • 2.3.6. Ionizing Radiation
  • 2.3.7. Immune System Activation
  • 2.3.8. Tumor Suppressor p53
  • 2.3.9. Epigenetic Modifications and mRNA Silencing
  • 2.4. Selective Capture of Autophagic Cargo in Mammals
  • 3. Tumor-Suppressive Roles for Autophagy in Cancer
  • 3.1. Genetic Basis for the Involvement of Autophagy in Tumor Suppression
  • 3.2. Inhibition of p62-Mediated Signaling Pathways
  • 3.3. Activation of Oncogene-Induced Senescence
  • 3.4. Maintenance of Immune Surveillance and Avoidance of Inflammation
  • 3.5. Clearance of Defective Mitochondria and Maintenance of Genomic Integrity
  • 3.6. Autophagy-Inducing Agents in Cancer Therapy
  • 4. Tumor-Promoting Roles for Autophagy in Cancer
  • 4.1. Genetic Evidence for the Involvement of Autophagy in Tumor Promotion
  • 4.2. Autophagy Supports Metabolic Adaptation to Accommodate Increased Biosynthetic Needs
  • 4.3. Survival Programs, Therapeutic Resistance, and Tumor Dormancy
  • 4.4. Interaction with the Tumor Microenvironment
  • 4.5. Autophagy-Inhibiting Agents in Cancer Therapy
  • 5. New Intersections Between Autophagy and Secretion
  • 5.1. Evidence for Autophagy-Dependent Secretion
  • 5.2. Emerging Roles for Autophagy-Dependent Secretion in Cancer
  • 6. Concluding Remarks and Perspectives
  • Acknowledgments
  • References
  • Chapter Two: Inhibitors of DNA Methylation, Histone Deacetylation, and Histone Demethylation: APerfect Combination for Ca...
  • 1. Introduction
  • 2. DNMTs: The Enzymes Responsible for DNA Methylation
  • 3. DNA-Demethylating Agents
  • 4. Azacytidine in RNA Metabolism
  • 5. Histone Acetylation
  • 5.1. Histone Deacetylases
  • 5.1.1. Class IHDACs
  • 5.1.2. Class II HDACs
  • 5.1.3. Class IV HDAC
  • 6. Nuclear Repressive Complexes
  • 6.1. Nucleosome Remodeling and Deacetylase Complex: ALink Between DNA Methylation, Histone Deacetylation, and Nucleosome ...
  • 6.2. NCoR and SMRT Corepressor Complex
  • 6.3. Corepressor of RE1-Silencing Transcription Factor (CoREST) Repressor Complex
  • 7. HDAC Inhibitors: General Mechanism of Zinc Chelators
  • 7.1. Mechanisms of HDAC-Induced Anticancer Effects
  • 7.2. Hydroxamic Acid-Based Inhibitors: Vorinostat and Panobinostat
  • 7.3. Benzamide-Based HDAC Inhibitor: Entinostat
  • 7.4. Cyclic Tetrapeptide-Based Inhibitor: Romidepsin
  • 7.5. Biomarkers of Response to HDAC Inhibition and Prognostic Indications
  • 8. Histone Methylation
  • 8.1. Histone Methyltransferases
  • 8.2. Histone Demethylation
  • 8.3. LSD1 Inhibitors
  • 8.3.1. MAO Inhibitors and Derivatives
  • 8.3.2. Polyamine Analogue-Based Inhibitors
  • 8.4. Cross-Talk Between HDACs and LSD1
  • 9. Experimental Evidence and Mechanisms by Which DNMT and HDAC Inhibitors Can Synergize to Reactivate Gene Expression: Ce...
  • 10. Experimental Evidence and Mechanisms by Which DNMT and HDAC or LSD1 Inhibitors CanSynergize to Reactivate Gene Expres...
  • 10.1. Chemosensitivity, Apoptotic Pathways, Inhibition ofTumor Growth
  • 10.2. Activation of Tumor Immune Response, Depletion of MDSCs, Tregs
  • 11. Summary
  • References
  • Chapter Three: Emerging Roles of Epigenetic Regulator Sin3 in Cancer
  • 1. Introduction
  • 2. Structure of Sin3 Protein and Core Complex
  • 3. Expression and Regulation
  • 4. Functions of Sin3 Protein
  • 5. Role of Sin3 in Cancer-Tumor Suppressor or Oncogene
  • 6. Sin3 Inhibits Invasion in Drosophila MEN2 Model
  • 7. Sin3B Promotes Senescence-Associated Inflammation and Pancreatic Cancer Progression
  • 8. Sin3A Promotes EMT and CSC-like Phenotype inTNBC
  • 9. Targeting Sin3A in Breast Cancer Using Small Molecule Mimetics of PAH2 Domain-Binding SID Motif
  • 10. Concluding Remarks: Challenges and Roadblocks in Developing Chromatin Modifiers as Drug Targets
  • Acknowledgments
  • References
  • Chapter Four: PAKs in Human Cancer Progression: From Inception to Cancer Therapeutic to Future Oncobiology
  • 1. Introduction
  • 2. Mechanism of Action
  • 3. Early Studies Connecting the PAK Family to Human Cancer
  • 4. Substrates Promoting Cytoskeleton Dynamic Invasion and Tumorigenesis
  • 5. Nuclear Signaling, Localization, and Functions
  • 6. Signaling Regulation of Gene Expression
  • 7. Coordinated Regulation of Translation, Transcription, and Splicing
  • 8. Modifier of ErbB2- and Wnt-Signaling
  • 9. Modulation of Angiogenesis Signaling
  • 10. Modifier of DNA Damage Response and Radiosensitivity
  • 11. Signaling Deregulation, Defective Mitotic and Human Cancer
  • 12. Regulation of Nuclear Receptor Signaling and Hormonal Response
  • 13. Signaling, Mammary Gland Development, and Breast Cancer
  • 14. Clinicopathological Features in Human Cancer
  • 14.1. Inflammation-Driven Cancers
  • 14.2. Amplification
  • 14.3. Co-overexpression
  • 15. Cancer Therapeutics Advances
  • 16. Conclusions and Prospective
  • Acknowledgments
  • References
  • Chapter Five: Sirtuins and the Estrogen Receptor as Regulators of the Mammalian Mitochondrial UPR in Cancer and Aging
  • 1. Introduction
  • 1.1. The Mitochondrial UPR vs Mitochondrial Retrograde Signaling Pathway or ROS Defense Pathway
  • 2. The Sirtuins
  • 3. UPRmt in Cancer: The Sirtuins and the UPRmt
  • 3.1. SIRT3 Is Downregulated in Cancer-Its Role as a Tumor Suppressor
  • 3.2. SIRT3 Is Upregulated by the UPRmt
  • 3.3. Reconciling the Up- and Downregulation of SIRT3 in Breast Cancer
  • 3.4. The SIRT1/FOXO Axis of the UPRmt in C. elegans
  • 3.5. The Sirtuins Axis of the UPRmt: A Unifying Model
  • 3.6. Evidences Supporting the Activation of UPRmt in Mouse Models of Cancer
  • 4. UPRmt in Cancer: The Estrogen Receptors and the UPRmt
  • 4.1. The Discovery of the Estrogen Receptor Arm of the UPRmt
  • 4.2. The IMS of the Mitochondria as a Sensitive Trigger of the UPRmt?
  • 4.3. Lyn Kinase, the New Kid on the Block of the ERa Axis of the UPRmt?
  • 4.4. The Intramitochondrial ERa and ERß: Link to the UPRmt?
  • 4.5. Mitochondrial ER Protects Against Apoptosis via Upregulation of SOD2 Activity
  • 5. Summary of the Roles of Sirtuins and the Estrogen Receptors in the UPRmt in Cancer
  • 6. UPRmt in Aging
  • 6.1. Inhibition of Mitochondrial Protein Translation Activates the UPRmt and Promotes Longevity
  • 6.2. Defect in the ETC Complexes Activates the UPRmt and Promotes Longevity
  • 6.3. SIRT1 and Aging
  • 6.4. SIRT3 and Aging
  • 6.5. SOD2 and Aging
  • 6.6. FOXO3a and Aging
  • 7. Summary of the Link Between the SIRT3/FOXO3a/SOD2 Axis of the UPRmt and Aging
  • 8. The Estrogen Receptors in Aging
  • 9. Sirtuins and Circadian Rhythm in Cancer and Aging
  • 10. Concluding Remarks
  • References
  • Chapter Six: Keratinocyte Carcinoma as a Marker of a High Cancer-Risk Phenotype
  • 1. Introduction
  • 2. Background and Descriptive Epidemiology ofKC
  • 2.1. KC Incidence and Mortality
  • 2.2. Primary Histological Types ofKC
  • 2.2.1. Basal Cell Carcinoma of theSkin
  • 2.2.2. Squamous Cell Carcinoma of theSkin
  • 2.3. The Occurrence of KC According to Person, Place, andTime
  • 2.3.1. Person: Demographic Characteristics
  • 2.3.2. Geographic Distribution ofKC
  • 2.3.3. Time Trends
  • 3. Determinants ofKC
  • 3.1. Host Factors Associated withKC
  • 3.1.1. SkinType
  • 3.1.2. Genetic Susceptibility
  • 3.1.2.1. Xeroderma Pigmentosum
  • 3.1.2.2. Epidermodysplasia Verruciformis
  • 3.1.3. Common, Low-Penetrant Genetic Variants Associated with KCRisk
  • 3.1.4. Immunosuppression
  • 3.1.5. Infections
  • 3.2. Environmental Risk Factors forKC
  • 3.2.1. Solar Ultraviolet Radiation
  • 3.2.2. Artificial Ultraviolet Radiation Exposure: Indoor Tanning
  • 3.2.3. Cigarette Smoking
  • 4. KC as a Marker of Increased Risk of Other Forms ofCancer
  • 4.1. Registry Studies
  • 4.2. Prospective Cohort Studies with Individual-LevelData
  • 4.3. Is the Association Between KC and Noncutaneous Malignancies Direct or Indirect?
  • 4.3.1. The Strength of the Evidence that KC is Associated with Increased Risk of Other Cancers
  • 4.3.2. KC and Risk of Other Cancers in Relation to the Multiple Primary CancerModel
  • 4.3.3. Why would KC be Associated with Increased Risk of Noncutaneous Malignancies?
  • 4.3.3.1. DNA Repair Gene Variants
  • 4.3.3.2. Inflammation and Immune Status
  • 5. Keratinocyte Carcinoma and Fatal Outcomes
  • 6. Overall Summary and Wrap-Up
  • References
  • Index
  • Color Plate
  • Back Cover

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