Klein | Advances in Cancer Research | E-Book | sack.de
E-Book

E-Book, Englisch, Band Volume 80, 223 Seiten, Web PDF

Reihe: Advances in Cancer Research

Klein Advances in Cancer Research


1. Auflage 2000
ISBN: 978-0-08-052438-2
Verlag: Elsevier Science & Techn.
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, Band Volume 80, 223 Seiten, Web PDF

Reihe: Advances in Cancer Research

ISBN: 978-0-08-052438-2
Verlag: Elsevier Science & Techn.
Format: PDF
Kopierschutz: 1 - PDF Watermark



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 including platelet-derived growth factor in disease, genetic predisposition in tumor development, primary effusion lymphoma, and many more. - Involvement of Platelet-Derived Growth Factor in Disease: Development of Specific Antagonists - Tumor Suppression Activity of Adenovirus E1a Protein: Anoikis and the Epithelial Phenotype - Comparative Analysis of the Transforming Mechanisms of EBV, KSHV, and HVS - Genetic Predisposition and Somatic Diversification in Tumor Development and Progression - Primary Effusion Lymphoma - A Liquid Phase Lymphoma of Fluid-Filled Body Cavities - The Dimensions of Antigen Recognition and the Levels of Immunological Specificity - Topoisomerase I-Mediated DNA Damage

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Weitere Infos & Material


1;Cover;1
2;Copyright Page;5
3;Contents;6
4;Contributors to Volume 80;10
5;Chapter 1. Involvement of Platelet-Derived Growth Factor in Disease: Development of Specific Antagonists;12
5.1;I. Introduction;13
5.2;II. Platelet-Derived Growth Factor (PDGF) and PDGF Receptors;14
5.3;III. Intracellular Signal Transduction;16
5.4;IV. In Vivo Function of PDGF;20
5.5;V. PDGF in Disease;24
5.6;VI. PDGF and PDGF Receptors as Drug Targets;30
5.7;VII. Future Perspectives;38
5.8;References;39
6;Chapter 2. Tumor Suppression Activity of Adenovirus E1a Protein: Anoikis and the Epithelial Phenotype;50
6.1;I. Introduction;50
6.2;II. Historical Development of E1a as a Tumor Suppressor;51
6.3;III. Epithelial Conversion: Phenomenology;52
6.4;IV. Epithelial Conversion: Mechanisms;52
6.5;V. Anoikis Sensitization and Tumor Suppression by E1a;55
6.6;References;57
7;Chapter 3. Comparative Analysis of the Transforming Mechanisms of Epstein–Barr Virus, Kaposi’s Sarcoma-Associated Herpesvirus, and Herpesvirus Saimiri;62
7.1;I. Introduction;62
7.2;II. Comparative Analysis of Gamma Herpesvirus Gene Products;66
7.3;III. Conclusion;83
7.4;References;84
8;Chapter 4. Genetic Predisposition and Somatic Diversification in Tumor Development and Progression;94
8.1;I. Introduction;95
8.2;II. Hereditary Colorectal Cancer Syndromes;96
8.3;III. Tumor Mutations and Molecular Clocks: Gateways to the Fourth Dimension;100
8.4;References;121
9;Chapter 5. Primary Effusion Lymphoma: A Liquid Phase Lymphoma of Fluid-Filled Body Cavities;126
9.1;I. Definition of Primary Effusion Lymphoma;127
9.2;II. Histogenes of Primary Effusion Lymphoma;130
9.3;III. Pathogenesis of Primary Effusion Lymphoma;132
9.4;IV. Epidemiology of Primary Effusion Lymphoma;144
9.5;V. Clinical Features of Primary Effusion Lymphoma;146
9.6;VI. Radioimaging of Primary Effusion Lymphoma;147
9.7;VII. Differential Diagnosis of Primary Effusion Lymphoma;147
9.8;VIII. Therapy of Primary Effusion Lymphoma;148
9.9;IX. Perspectives;149
9.10;References;151
10;Chapter 6. Dimensions of Antigen Recognition and Levels of Immunological Specificity;158
10.1;I. Introduction;159
10.2;II. Logical Preliminaries: Boundaries of Categories and Categories of Boundaries;160
10.3;III. Monovalent Recognition;164
10.4;IV. Multivalent Recognition;176
10.5;V. Specificity of Cellular Activation;182
10.6;VI. Organismal Specificity;185
10.7;VII. Conclusions;193
10.8;References;194
11;Chapter 7. Topoisomerase I-Mediated DNA Damage;200
11.1;I. Introduction;200
11.2;II. Structural Domains of Top1;201
11.3;III. Top1 Functions and Protein Interactions;202
11.4;IV. The Top1 Catalytic Cycle and Cleavage Complexes;206
11.5;V. Anticancer Top1 Poisons;209
11.6;VI. Suppression and/or Enhancement of Top1 Cleavage Complexes by DNA Damage;212
11.7;VII. Processing of Top1-Mediated Dna Lesions;220
11.8;VIII. Conclusions;222
11.9;References;222
12;Index;228



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