Klein Advances in Cancer Research

1. Auflage 2001
ISBN: 978-0-08-052228-9
Verlag: Elsevier Science & Techn.
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, Band Volume 83, 261 Seiten, Web PDF

Reihe: Advances in Cancer Research

The Advances in Cancer Research series provides invaluable information on the exciting and fast-moving field of cancer research. This volume presents outstanding and original reviews on a variety of topics, including suppressor and oncogenic roles of TGF-b and its signaling pathways in tumorigenesis, hereditary diffuse gastric disease, the role of heparan sulfate proteoglycans in cell signaling and cancer, V-gene mutations in B-cell-derived human malignancy, MHC antigens and tumor escape from immune surveillance, the role of selection in progressive neoplastic transformation, and the genomic stability, neuronal development, and cancer cross paths of ATM. - Suppressor and Oncogenic Roles of TGF-aand Its Signaling Pathways in Tumorigenesis - Hereditary Diffuse Gastric Disease - Role of Heparan Sulfate Proteoglycans in Cell Signaling and Cancer - The Occurrence and Significance of V-Vene Mutations in B Cell-Derived Human Malignancy - MHC Antigens and Tumor Escape from Immune Surveillance - Foundations in Cancer Research: The Role of Selection in Progressive Neoplastic Transformation - ATM: Genomic Stability, Neuronal Development, and Cancer Cross Paths

Autoren/Hrsg.

Klein, George

Inhaltsverzeichnis

1;Cover;1
2;Title Page;4
3;Copyright Page;5
4;Contents;6
5;Contributors to Volume 83;10
6;Chapter 1. Suppressor and Oncogenic Roles of Transforming Growth ß and Its Signaling Pathways in Tumorigenesis;12
6.1;I. Introduction;13
6.2;II. The Tgf-ß Signaling Pathway;14
6.3;III. Bimodal Action of Tgf-ß in Tumorigenesis;25
6.4;IV. Activities of Tgf-ß Important for Oncogenesis;29
6.5;V. Dysregulated Expression or Activity of Components of Tgf-ß Signaling Pathways in Oncogenesis;44
6.6;VI. Summary;52
6.7;References;53
7;Chapter 2. Hereditary Diffuse Gastric Cancer;66
7.1;I. Introduction;66
7.2;II. Hereditary Diffuse Gastric Cancer;67
7.3;III. Mutations in CDH-1;69
7.4;IV. The Tumor Spectrum of Hdgc;71
7.5;V. Inactivation of the Second CDH-1 Allele;71
7.6;VI. Molecular Mechanism of Hdgc Susceptibility;72
7.7;VII. Clinical Criteria and Management of Hdgc;73
7.8;VIII. Conclusion;74
7.9;References;74
8;Chapter 3. Role of Heparan Sulfate Proteoglycans in Cell Signaling and Cancer;78
8.1;I. Introduction;78
8.2;II. Hspgs and Cancer;80
8.3;III. Fgf Signaling and Hspgs in Drosophila;82
8.4;IV. Dpp Signaling and Hspgs in Drosophila;84
8.5;V. Wg and Hh Signaling and Hspgs in Drosophila;84
8.6;VI. The Role of Glypicans in Wg Signaling;86
8.7;VII. Hspgs Are Involved in Hh Movement;88
8.8;VIII. Conclusion;89
8.9;References;90
9;Chapter 4. The Occurrence and Significance of V Gene Mutations in B Cell–Derived Human Malignancy;92
9.1;I. Introduction;93
9.2;II. Immunoglobulin Genes in Normal B Cell Development;94
9.3;III. Immunoglobulin Genes in B Cell Tumors;101
9.4;IV. Somatic Mutation in B Cell Tumors;103
9.5;V. Chronic Lymphocytic Leukemia;106
9.6;VI. Follicular Lymphoma;111
9.7;VII. Diffuse Large B Cell Lymphoma;113
9.8;VIII. Plasma Cell Tumors;115
9.9;IX. Conclusion;120
9.10;References;121
10;Chapter 5. Mhc Antigens and Tumor Escape from Immune Surveillance;128
10.1;I. Introduction;128
10.2;II. Hla Class I Antigen Expression in Primary Tumors;130
10.3;III. Changes in MHC Class I Antigen Expression during Metastatic Colonization;150
10.4;IV. T Cell Immunoselection of MHC Class I–Negative Tumor Clones;152
10.5;V. Expression of Nonclassical Hla Class I Molecules in Tumors;154
10.6;VI. Tumor Nk Escape Mechanisms;156
10.7;VII. Hla Class I Loss and T Cell–Based Immunotherapy;157
10.8;VIII. Hla Class II Antigens in Tumors;158
10.9;IX. Conclusions;160
10.10;References;162
11;Chapter 6. The Role of Selection in Progressive Neoplastic Transformation;170
11.1;I. Introduction;171
11.2;II. Spontaneous Neoplastic Transformation in Cell Culture;173
11.3;III. Selection in Transformation of Established Cell Lines;179
11.4;IV. The Contribution of Apoptosis to Selection in Neoplastic Transformation;195
11.5;V. Inhibition of Growth of Transformed Cells by Surrounding Nontransformed Cells;198
11.6;VI. Confounding Effects of Variable Cell Behavior on the Dynamics of Transformation;199
11.7;VII. Summary of the Major Features of Spontaneous Transformation;199
11.8;VIII. Evidence for Selection in Experimental and Human Cancer;201
11.9;IX. Sources of Genetic Variation for Possible Selection in Tumor Development;206
11.10;X. The Nature of Selection in Vivo;207
11.11;XI. Selection in Carcinogenesis by Polycyclic Aromatic Hydrocarbons;210
11.12;XII. Conclusions;212
11.13;References;213
12;Chapter 7. Atm Genome Stability, Neuronal Development, and Cancer Cross Paths;220
12.1;I. Introduction;221
12.2;II. Ataxia-Telangiectasia A Disease Caused by Atm Deficiency;222
12.3;III. The Atm Gene and Its Mutations;227
12.4;IV. The Atm Protein From Sequence to Function;229
12.5;V. Atm Functions Lessons from Knockout Mice;242
12.6;VI. Atm Deficiency Leads to Increased Oxidative Stress;249
12.7;VII. Atm Interplay with Signaling Pathways Associated with Growth and Differentiation;251
12.8;VIII. Defects in Dna Damage Response and Cancer Predisposition;252
12.9;IX. Conclusions;254
12.10;References;255
13;Index;266