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Without metastasis, prostate cancer would be both tolerable and treatable. The high incidence of indolent and organ confined disease is testament to this sweeping generalisation. Equally, if molecular markers of metastatic spread can be identified, then the choice of treatment for many patients would be easier and more radical, even curative. However, should prevention and treatment of the primary tumors prove difficult or impossible, then a knowledge of the phenotype of advanced metastatic tumors should allow us to target these lesions for destruction by conventional (drug based) or more innovative means such as gene and/or immunotherapy (1). The process of metastasis has been reviewed many times (e. g. , 2) and has been subdivided for ease of analysis into a number of discrete stages (see Figure 1). It has been suggested that at least 10 separate genetic 2. ECM degradation: migration MMP ; Integrin ; TIMP 3. Intravasation MMP TIMP 1. Cellular independence 4. Transport Adhesion loss and evasion (E Cadherin ) of host immune system MHCClass1 ICAM-1 to block T cell receptor 5. Arrest of movement: endothelial adhesion CD44 or switch 6. Extravasation to colonise new site 7. Proliferation at Laminin R distant site to form Integrin switch METASTASIS Figure 1. Stages in prostate cancer metastasis. Basic processes in tumor metastases are indicated in the boxes with some key changes in gene expression indicated at each stage by the solid arrows.
Table des matières
Chapter 1: Introduction: Metastasis as a Therapeutic Target
Richard J. Ablin and Malcolm D. Mason
Chapter 2: The Natural History of Prostate Cancer
David F. Penson and Peter C. Albertsen
Chapter 3: The Search for Genes Which Influence Prostate Cancer Metastasis: A Moving Target?
Norman J. Maitland
Chapter 4: Polyunsaturated Fatty Acids and Prostate Cancer Metastasis
Wen G. Jiang
Chapter 5: Role of Prostaglandin Synthesis and Cyclooxygenase-2 in Prostate Cancer and Metastasis
Alaa F. Badawi
Chapter 6: Cell Cycle Regulation
Ruchi M. Newman and Bruce R. Zetter
Chapter 7: Epithelial-Mesenchymal Molecular Interactions in Prostatic Tumor Cell Plasticity
Mary J.C. Hendrix, Jun Luo, Elisabeth A. Seftor, Navesh Sharma, Paul M. Heidger
Jr., Michael B. Cohen, Robert Bhatty, Jirapat Chungthapong, Richard E.B. Seftor, and David Lubaroff
Chapter 8: Orthotopic Metastatic Mouse Models of Prostate Cancer
Robert M. Hoffman
Chapter 9: ß-Catenin, its Binding Partners and Signalling Mechanisms: Implications in Prostate Cancer
Gaynor Davies, Gregory M. Harrison, and Malcolm D. Mason
Chapter 10: Hepatocyte Growth Factor/Scatter Factor and Prostate Cancer Metastasis
Gaynor Davies, Wen G. Jiang, and Malcolm D. Mason
Chapter 11: Matrix Degradation in Prostate Cancer
Michael J. Wilson and Akhouri A. Sinha
Chapter 12: The Biology of Bone Metastases from Prostate Cancer and the Role of Bisphosphonates
Noel W. Clarke and Herbert A. Fleisch
Chapter 13: Non-Steroidal Anti-Androgen Use as Part of Combined Androgen Blockade Therapy for Metastatic or Locally Advanced Prostate Cancer: a Review of the Evidence on Efficacy and Toxicity
Mike Shelley, Charles Bennett, Derek Nathan, and Oliver Sartor
Chapter 14: Strategies for the Implementation of Chemotherapy and Radiotherapy
Paula Scullin, Joe M. O'Sullivan, and Christopher C. Parker
Chapter15: Immuno-gene Therapy for Metastatic Prostate Cancer
Takefumi Satoh, Terry L. Timme, Yehoshua Gdor, Brian J. Miles, Robert J. Amato, Dov Kadmon, and Timothy C. Thompson
Chapter 16: Distilling the Past - Envisioning the Future
Richard J. Ablin and Malcolm D. Mason
Résumé
Without metastasis, prostate cancer would be both tolerable and treatable. The high incidence of indolent and organ confined disease is testament to this sweeping generalisation. Equally, if molecular markers of metastatic spread can be identified, then the choice of treatment for many patients would be easier and more radical, even curative. However, should prevention and treatment of the primary tumors prove difficult or impossible, then a knowledge of the phenotype of advanced metastatic tumors should allow us to target these lesions for destruction by conventional (drug based) or more innovative means such as gene and/or immunotherapy (1). The process of metastasis has been reviewed many times (e. g. , 2) and has been subdivided for ease of analysis into a number of discrete stages (see Figure 1). It has been suggested that at least 10 separate genetic 2. ECM degradation: migration MMP ; Integrin ; TIMP 3. Intravasation MMP TIMP 1. Cellular independence 4. Transport Adhesion loss and evasion (E Cadherin ) of host immune system MHCClass1 ICAM-1 to block T cell receptor 5. Arrest of movement: endothelial adhesion CD44 or switch 6. Extravasation to colonise new site 7. Proliferation at Laminin R distant site to form Integrin switch METASTASIS Figure 1. Stages in prostate cancer metastasis. Basic processes in tumor metastases are indicated in the boxes with some key changes in gene expression indicated at each stage by the solid arrows.
