| Description |
1 online resource (approximately 380 pages) |
| Series |
Cancer Metastasis - Biology and Treatment, 1568-2102 ; 10 |
|
Cancer metastasis (Series) ; 10. 1568-2102
|
| Contents |
Front Matter; Introduction: Metastasis as a Therapeutic Target; The Natural History of Prostate Cancer; The Search for Genes Which Influence Prostate Cancer Metastasis: A Moving Target?; Polyunsaturated Fatty Acids and Prostate Cancer Metastasis; Role of Prostaglandin Synthesis and Cyclooxygenase-2 in Prostate Cancer and Metastasis; Cell Cycle Regulation; Epithelial-Mesenchymal Molecular Interactions in Prostatic Tumor Cell Plasticity; Orthotopic Metastatic Mouse Models of Prostate Cancer; ß-Catenin, its Binding Partners and Signalling Mechanisms: Implications in Prostate Cancer |
|
Hepatocyte Growth Factor/Scatter Factor and Prostate Cancer MetastasisMatrix Degradation in Prostate Cancer; The Biology of Bone Metastases from Prostate Cancer and the Role of Bisphosphonates; 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; Strategies for the Implementation of Chemotherapy and Radiotherapy; Immuno-gene Therapy for Metastatic Prostate Cancer; Distilling the Past -- Envisioning the Future; Back Matter |
| Summary |
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 |
| Analysis |
neoplasms |
|
biomedische wetenschappen |
|
biomedicine |
|
Medicine (General) |
|
Geneeskunde (algemeen) |
| Bibliography |
Includes bibliographical references and index |
| Notes |
English |
|
Print version record |
| Subject |
Prostate -- Cancer -- Research
|
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Metastasis -- Diagnosis
|
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Metastasis -- Research -- Methodology
|
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Metastasis.
|
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Neoplasm Metastasis
|
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Prostatic Neoplasms
|
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MEDICAL -- Oncology.
|
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HEALTH & FITNESS -- Diseases -- Cancer.
|
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Biomédecine.
|
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Sciences de la vie.
|
|
Metastasis
|
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Prostate -- Cancer -- Research
|
| Form |
Electronic book
|
| Author |
Ablin, Richard J., 1940-
|
|
Mason, Malcolm (Malcolm D.)
|
| ISBN |
9781402058479 |
|
1402058470 |
|
9781402058462 |
|
1402058462 |
|
9786611067243 |
|
6611067248 |
|
1281067245 |
|
9781281067241 |
|
