Drug Resistant Neoplasms.

Intro -- DRUG RESISTANT NEOPLASMS -- Contents -- Preface -- Therapeutic Implications of theIntrinsic and Acquired Resistance ofCancer Stem/Progenitor Cells inInefficacy of Current CancerTreatments and Disease Relapse -- Abstract -- Abbreviations -- Introduction -- Functions of Tumorigenic and Migrating CancerStem/Progenitor Cells in Cancer Initiation,Progression and Metastases -- Molecular Transforming Events in Cancer Stem/Progenitor Cells and TheirProgenies Associated with Tumor Development -- Molecular Events Associated With the EMT Process, Invasion andMetastasis of Cancer Stem/Progenitor Cells -- Intrinsic and Acquired Phenotypes of CancerStem/Progenitor Cells Associated with TheirResistance to Current Cancer Treatments -- Heterogeneity of Cancers Derived from Distinct Tumorigenic and MigratingCancer Stem/Progenitor Cells and Their Differential Response to CurrentClinical Treatments -- Current Cancer Therapies -- Novel Cancer Therapies by Targeting Tumor- andMetastasis-Initiating Cells and TheirMicroenvironment -- Molecular Targeting of Tumorigenic and MigratingCancer Stem/Progenitor Cells -- Molecular Targeting of the Local Microenvironment of Tumorigenic andMigrating Cancer Stem/Progenitor Cells -- Conclusions -- Acknowledgments -- References -- Role of O6-Methyl Guanine-DNA MethylTransferase and the Effect of O6-Benzylguanine inCancer Chemotherapy -- Abstract -- Alkylating Agents in Cancer Chemotherapy -- O6-Methyl Guanine-DNA MethylTransferase (MGMT) -- Loss of MGMT: Epigenetics -- Loss of MGMT and/or DNA Mismatch Repair inAlkylation Tolerance -- Loss of MGMT in G to a Transition Mutation -- O6-Benzylguanine, a Nearly Non-ToxicMGMT Inhibitor -- O6-Benzylguanine as a Cell Cycle Inhibitor -- O6-Benzylguanine: Its Limitation -- O6-Benzylguanine Analogues, O6-Benzyl-2'-Deoxyguanosine (Dbg).

O6-Benzylguanine: A Modulator toOvercome Drug Resistance -- O6-Benzylguanine/ MGMT in Relation with Cis-Diamminedichloroplatinum II (Cisplatin, CDDP)Treatment -- 1). The Widely used Anticancer Drug CDDP -- 2) Modulators for CDDP -- 3) MGMT Predictive Chemosensitivity for CDDP -- 4) CDDP Attenuates MGMT Expression -- 5) O6-Benzylguanine Enhances the Cytotoxicity Of CDDP -- 6). How does CDDP Attenuate MGMT Expression? -- 7). Which Pathways are Involved in O6-Benzylguanine EnhancedCytotoxicity of CDDP? -- O6-Benzylguanine/ MGMT in Relationto 5-Fluorouracil (5-FU) Treatment -- 1). The Widely used Anticancer Drug 5-FU -- 2). MGMT and O6-Benzylguanine in the Cytotoxicity of 5-FU -- 3). Which Pathways are Involved in O6-Benzylguanine-EnhancedCytotoxicity of 5-FU? -- References -- The Role of TumouralMicroenvironment and Its Vasculaturein Chemotherapy Drug Resistance:The Potential for Its Modulation toAchieve Therapeutic Gain -- Introduction -- Tumour Interstitial Pressure -- Clinical Sequelae: Prognostic Significance ofThese Changes -- Drug Activity -- Therapeutic Agents Being Evaluated in the Clinic:Highlights and Promising Results -- Hypoxia -- Hypoxia: Definition and Its Causes -- The Tumour Cells' Response to Hypoxia -- The Evaluation of Hypoxia and Its PrognosticImportance -- Hypoxia and Resistance to Therapy -- Therapies Directed to Hypoxia -- Drug Penetration -- Summary -- References -- Inherent and Microenvironment-Mediated Mechanisms of DrugResistance -- Abstract -- Introduction -- Conclusion -- References -- Studies on the Mechanisms of AcquiredResistance to EGFR Tyrosine KinaseInhibitor Gefitinib in NSCLC Cell Lines:Evidence that Ligand-InducedEndocytosis of EGFR via the Early/LateEndocytic Pathway is Associated withGefitinib Sensitivity of NSCLC Cell Line -- Abstract -- Introduction -- Results.

Intracellular Distribution of EGFR and pEGFR between the Gefitinib-Sensitive or Gefitinib-Resistant NSCLC Cell Lines -- Aggregated Vesicular Structures of Early Endocytic Compartments AreFound to be Overlapped With Sorting Nexin 1 (SNX1) Localized in thePerinuclear Region of Gefitinib-Resistant NSCLC Cell Line -- Ligand-Induced EGFR Endocytosis Operates Normally via the Early/LateEndocytic Pathway in the Gefitinib-Sensitive NSCLC Cell Line, however,Aberrant Endocytosis of EGFR Occurs in the Gefitinib-Resistant NSCLC CellLine -- Gefitinib Impedes Endocytosis of Ligand-Induced Phosphorylated EGFR viathe Early Endocytic Pathway in NSCLC Cell Lines -- Phosphorylated EGFR Is Efficiently Trafficked to Late Ensosmes via EarlyEndosmes in the Gefitinib-Sensitive NSCLC Cell Line, however anAccumulation of Phosphorylated EGFR Is Observed in the EarlyEndosomes instead of its Delivery to Late Endosomes in Gefitinib-Resistant NSCLC Cell Line -- Discussion -- Conclusion -- References -- Mechanisms of Resistance to EGFReceptor-Tyrosine Kinase Inhibitor inNSCLC Cell Lines: Gefitinib Sensitivityis Closely Correlated with Ligand-Induced Endocytosis of PhosphorylatedEGF Receptor -- Abstract -- Introduction -- Results -- Phosphorylated EGFR is Localized in the Cytosol and the Nucleus inGefitinib-Sensitive or Gefitinib-Resistant NSCLC Cell Lines -- Early Endosomes Forms Aggregated Vesicular Structures which areAssociated with Sorting Nexin 1 (SNX1) in Gefitinib-Resistant NSCLCCell Line -- Rapid Endocytosis of Phosphorylated EGFR via the Early/Late EndocyticPathway in the Gefitinib-Sensitive NSCLC Cell Line -- Phosphorylated EGFR is Efficiently Endocytosed and Trafficked to LateEndosomes/Lysosomes in the Gefitinib-Sensitive NSCLC Cell Line -- Discussion -- Materials and Methods -- Materials -- Cell Culture -- Antibodies -- Immunofluorescence Microscopy -- Abbreviations.

References -- Targeting Adverse Features ofHormone-Resistant Breast Cancer -- Abstract -- 1. Introduction -- 2. Endocrine Resistance Is Accompanied by anAdverse Cellular Phenotype -- 2.1. Endocrine Resistant Breast Cancer Cells Overexpress Cell SurfaceReceptors That May Sensitize Them to the Tumour Microenvironment -- 2.1.1. c-Met Receptor -- 2.1.2. CD44 -- 3. Antihormones Induce Pro-Invasive Responsesduring the Drug-Responsive Phase Which, in theAppropriate Cell Context, May Contribute to anAdverse Cell Phenotype -- 4. A Role for Src in Endocrine-Sensitive andEndocrine-Resistant Breast Cancer -- 4.1. Endocrine-Sensitive Breast Cancer -- 4.2. Endocrine-Resistant Breast Cancer -- Conclusions -- References -- Systematic Analysis of Patterns ofCross Resistance between AnticancerAgents -- Abstract -- Introduction -- Patterns of Cross Resistance -- Complete Cross Resistance -- Incomplete Cross Resistance -- Inverse Resistance -- Conclusions -- References -- Molecular Structure and Energy:Clinical Importance in Drug-ResistantNeoplasms -- Abstract -- Introduction -- Drug-Resistant Neoplasms:General Considerations -- Drug-Resistant Neoplasms: Molecular Structure -- Drug-Resistant Neoplasmd: Energy -- References -- Treating Drug-Resistant Malignancy -- Abstract -- Introduction -- Classical Way to Treat Drug-Resistant Malignancy -- New Ways to Treat Drug-Resistant Malignancy -- A. Gene therapy -- B. Nanotherapy -- C. Immunotherapy -- Some Facts on Reported Data forDrug-Resistant Cancer -- A. Sponsorship in Clinical Trial Report: Ethical Concerns -- B. Problems with a Double Standard -- References -- Overcoming Ovarian Cancer DrugResistance with Phytochemicals andother Compounds∗ -- Abstract -- Introduction -- Clinical Presentation -- Treatment -- Drug Resistance -- Genomics and Proteomics -- Molecular Mechanisms -- Potential Therapies -- Clinical Trials.

Experimental Studies -- Phytochemicals -- Polyphenols -- Resveratrol -- Quercetin -- Curcumin -- Epigallocatechin-3-Gallate -- Conclusion -- Acknowledgments -- References -- New Research Communications onCancer Drug Resistance, Assessmentof Cancer Drug Resistancewith Nuclear Medicine Images∗ -- Abstract -- I. Introduction -- II. PET Studies -- 1. Pharmacokonetic Assessment -- 2. Metabolic Assessment -- 3. Environmental Resistance -- 3.1. Blood Flow -- 3.2. Hypoxia -- 3.3. Angiogenesis -- 4. Cellular Resistance -- 4.1. Multi-Drug Resistance (MDR) -- 4.2. Rapid Cell Proliferation -- 4.3. Apoptosis -- 4.4. DNA Repair -- 4.5. Drug Receptor Interaction -- III. SPET Studies -- 1. Thallium-201 -- 2. MDR -- 3. Hypoxia -- 4. Other SPET Tracers -- IV. Conclusion -- References -- Index.

Description based on publisher supplied metadata and other sources.

Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, 2024. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries.