rdf-syntax-grammar
mods:
  schema location: http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
  title info:
    title: Advances in cancer research
    part number: Volume 138
  name:
    name part: Tew, Kenneth D.
    role:
      role term: editor.
  name:
    name part: Fisher, Paul B.
    role:
      role term: editor.
  name:
    name part: ScienceDirect (Online service)
  type of resource: text
  genre: bibliography
  genre: Electronic books.
  origin info:
    place:
      place term: cau
    date issued: 2018
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: remote
    extent: 1 online resource
  abstract: Advances in Cancer Research, Volume 138, the latest release in this ongoing, well-regarded serial provides invaluable information on the exciting and fast-moving field of cancer research. This volume presents original reviews on research bridging oncology and gene expression, with this volume covering unconventional approaches to modulating the immunogenicity of tumor cells, tumor dormancy and immunoediting, the emerging role of anti-apoptotic Bcl-2 family proteins in chemoresistance, Beclin-1 and autophagy, MDA-7/IL-24, and nanotechnology and medicine.
  table of contents: Front Cover; Advances in Cancer Research; Copyright; Contents; Contributors; Chapter One: Leveraging Epigenetics to Enhance the Cellular Response to Chemotherapies and Improve Tumor Immunogenicity; 1. Introduction; 1.1. Chemotherapy and the Induced Immune Response; 1.2. The Value of Chemosensitization; 1.3. Targeting Epigenetics to Achieve Chemosensitization; 2. Targeting Epigenetic Regulators to Achieve Sensitization to ICD-Inducing Chemotherapies; 2.1. Writers; 2.1.1. Histone Acetyltransferases; 2.1.2. Histone Methyltransferases; 2.1.3. DNA Methyltransferases; 2.2. Erasers.
  table of contents: 2.2.1. Histone Deacetylases2.2.2. Histone Demethylases; 2.2.3. TET Family of DNA Demethylases; 2.3. Readers; 2.3.1. Bromodomains; 2.3.2. Chromodomain Helicase DNA-Binding Proteins; 2.4. miRNAs; 3. Conclusions and Future Directions; Acknowledgments; Conflicts of Interest; References; Chapter Two: VDAC Regulation: A Mitochondrial Target to Stop Cell Proliferation; 1. Introduction; 1.1. Mitochondria, Energy Production, and Biosynthesis; 1.2. Bioenergetics and Biosynthesis in the Warburg Phenotype; 1.3. Mechanisms to Suppress Mitochondrial ATP Production: A Drive on Glycolysis.
  table of contents: 2. VDAC Channels and Mitochondrial Metabolism2.1. The MOM: A VDAC-Containing Interphase to Modulate Cellular Bioenergetics; 2.2. VDAC Structure and Regulation of the Conductance; 3. VDAC-Tubulin Interaction; 3.1. VDAC Inhibition by Free Tubulin; 3.2. VDAC-Tubulin Modulation of Cellular Bioenergetics During Cell Cycle; 4. Tumor Metabolic Flexibility: Advantages of Targeting Metabolism in Chemotherapy; 5. VDAC-Tubulin Antagonists: A Strategy for Opening VDAC; 5.1. Erastin and VDAC-Tubulin Antagonists; 5.2. VDAC Opening, Glycolysis, and Reactive Oxygen Species Formation.
  table of contents: 5.3. VDAC-Dependent Metabolic Hits: Anti-Warburg Effect and Oxidative Stress6. Concluding Remarks; Acknowledgment; References; Chapter Three: Acquired Resistance to Drugs Targeting Tyrosine Kinases; 1. Introduction; 2. Inhibition of Bcr-Abl and Nonreceptor Tyrosine Kinases; 2.1. Mechanisms of Acquired vs Intrinsic Resistance to TKIs; 2.2. Acquired Resistance to Abl Kinase TKIs; 3. Receptor and Nonreceptor Tyrosine Kinases Activate Common Pathways; 4. Receptor TKIs and the EGFR Family; 4.1. Lapatinib, a Dual Kinase Inhibitor of EGFR and HER2, and Afatinib, a Covalent ErbB1 RTKI.
  table of contents: 4.2. Lapatinib-Induced Kinome Reprogramming and Its Role in Resistance5. Epigenetic Mechanisms of Resistance; 5.1. Resistance to Receptor TKIs vs Receptor-Targeted Antibodies: IGF-1R; 5.2. Other mAbs and Acquired Resistance: Trastuzumab; 6. IGF-1R and Dependence Receptors in Drug Resistance; 7. Conclusions and Future Perspective; Acknowledgments; References; Chapter Four: Extracellular-Regulated Kinases: Signaling From Ras to ERK Substrates to Control Biological Outcomes; 1. Introduction; 2. Identification of Extracellular-Regulated Kinases; 3. Ras to MAP Kinase Kinases.
  note: edited by Kenneth D. Tew, Paul B. Fisher.
  note: Includes bibliographical references.
  subject:
    topic: Cancer
    topic: Research
  subject:
    topic: Cancer
    topic: Recherche
  subject:
    topic: HEALTH & FITNESS
    topic: Diseases
    topic: General
  subject:
    topic: MEDICAL
    topic: Clinical Medicine
  subject:
    topic: MEDICAL
    topic: Diseases
  subject:
    topic: MEDICAL
    topic: Evidence-Based Medicine
  subject:
    topic: MEDICAL
    topic: Internal Medicine
  subject:
    topic: Cancer
    topic: Research
  classification: RC267
  classification: 616.9940072
  related item:
    title info:
      title: Advances in cancer research. Volume 138
    origin info:
      publisher: San Diego : Elsevier Science, 2018
  related item:
    title info:
      title: Advances in cancer research ; v. 138
  identifier: 9780128151280
  identifier: 0128151285
  identifier: 0128151277
  identifier: 9780128151273
  identifier: 9780128151280 Ingram Content Group
  identifier: http://proxy.library.tamu.edu/login
  record info:
    record content source: N$T
    record creation date: 180320
    record change date: 20260327153239.1
    record identifier: in00005763289
    language of cataloging:
      language term: eng