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Chapter One. Understanding the Role of ETS-Mediated Gene Regulation in Complex Biological Processes
2 Modulation of ETS Function
3 Defining and Characterizing ETS Target Genes
4 ETS and MicroRNA
5 ETS Mouse Knockout and Mutant Models
6 ETS Factors and Cancer
7 The Role of ETS Factors in the Microenvironment
8 ETS Factors and Other Diseases
9 Targeting the ETS Network
10 Concluding Remarks
Chapter Two. Advances in Understanding the Coupling of DNA Base Modifying Enzymes to Processes Involving Base Excision Repair
2 Enzymes That Modify Bases in DNA
3 The Removal of Enzymatically Modified Bases by BER
4 Relationships Between the Activity of Base Modifying Enzymes and DNA Repair
Chapter Three. Role of Oxidative Stress and the Microenvironment in Breast Cancer Development and Progression
1 Oxidative Stress Changes the Breast Tumor Microenvironment
2 Oxidative Stress Regulate Caveolin-1 Signaling and Energy Metabolism in the Tumor Microenvironment
3 Oxidative Stress Causes Fibroblasts to Undergo Senescence and Induces Mitochondrial Dysfunction
4 Conclusions and Future Perspectives—Should We Target Breast Cancer Stroma?
Chapter Four. Mitochondrial Alterations During Carcinogenesis: A Review of Metabolic Transformation and Targets for Anticancer Treatments
1 An Overview of the Role of Mitochondria in Cancer
2 Alterations in Energy Metabolism in Cancer Cells
3 Oncogenes and Tumor Suppressors Involved in Mitochondrial Function
4 Mitochondria as the Key Organelles Involved in Cell Death and Survival
5 Cancer Metastasis: Implication of Mitochondrial Metabolism in the Adaptation to Microenvironment
6 Diagnostic and Therapeutic Applications of Metabolic Transformation
7 Concluding Remarks
Chapter Five. Human Polynucleotide Phosphorylase (hPNPaseold-35): Should I Eat You or Not—That Is the Question?
1 RNA Degradation Pathways
4 Identification and Regulation of hPNPaseold-35 Expression
5 Subcellular Localization of hPNPaseold-35
6 Evolution of PNPases
7 Functions of hPNPaseold-35
8 Functions of hPNPaseold-35 in Mitochondria
9 Concluding Remarks
Chapter Six. FOXM1 (Forkhead box M1) in Tumorigenesis: Overexpression in Human Cancer, Implication in Tumorigenesis, Oncogenic Functions, Tumor-Suppressive Properties, and Target of Anticancer Therapy
1 FOXM1 Overexpression in Tumor Cells
2 FOXM1 in Tumorigenesis
3 The Unexpected Tumor Suppressor Role of FOXM1
4 Context-Dependent Effects of FOXM1
5 FOXM1 as Target for Anticancer Therapy
Chapter Seven. Therapeutic Cancer Vaccines: Past, Present, and Future
2 Tumor Cell Vaccines
3 DC Vaccines
4 Protein/Peptide-Based Cancer Vaccines
5 Genetic Vaccines
6 Cancer Vaccine Therapy Combined with Other Treatment Modalities
7 Lessons Learned from Cancer Vaccine Trials
8 Tumor-Induced Immune Suppression and TME
9 Concluding Remarks
Advances in Cancer Research provides invaluable information on the exciting and fast-moving field of cancer research. Here, once again, outstanding and original reviews are presented on a variety of topics.
Researchers and students in the basic and clinical sciences of cancer biology and oncology, plus related areas in genetics, immunology, pharmacology, cell biology, and molecular biology.
- No. of pages:
- © Academic Press 2013
- 5th July 2013
- Academic Press
- Hardcover ISBN:
- eBook ISBN:
Praise for the Serial
"This classic and essential series presents critical overviews on select aspects of both cancer research and the basic underlying sciences." --American Scientist
"Excellent, highly informative, in-depth reviews…expertly written, up-to-date, and well-referenced." --Journal of Medicinal Chemistry
"This is a series that has a long tradition of excellence in the field of cancer biology." --Doody’s Publishing Reviews
Professor & Chairman, Dept of Cell & Molecular Pharmacology John C. West Chair of Cancer Research, Medical University of South Carolina, USA
The Tew laboratory maintains an interest in using redox pathways as a platform to develop therapeutic strategies through drug discovery/development and biomarker identification. We interrogate how reactive oxygen and nitrogen species (ROS/RNS) impact cancer cells and develop novel drugs that impact on glutathione based pathways. Our research efforts have been integral to studies that have identified glutathione S-transferases (GST) as important in drug resistance, catalytic detoxification and as arbiters of kinase-mediated cell signaling events. In addition, we have been instrumental in defining how GSTP contributes to the process by which cells respond to ROS by selective addition of glutathione to specific protein clusters, so called S-glutathionylation. Each of these research areas has had broad impact on a number of cancer disciplines. Moreover, we have also been seminally involved in the Phase I to III clinical testing of three oncology drugs, Telcyta, Telintra and NOV-002. Other ongoing translational efforts have produced two ongoing clinical trials to measure the effectiveness of serum S-glutathionylated serine proteinase inhibitors as possible biomarkers for exposure to hydrogen peroxide mouthwashes and radiation.
Department of Cell and Molecular Pharmacology, Medical University of South Carolina, USA
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