Descripción del título
Metastasis of prostate canc...
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
Monografía
monografia Rebiun25650272 https://catalogo.rebiun.org/rebiun/record/Rebiun25650272 m o d cr cn||||||||| 080107s2007 ne ob 001 0 eng d 234238164 316684230 317359150 437206843 466085616 607255536 613461351 648326473 739172409 756425534 985052342 987728473 994692486 1005782122 1020000566 1035662784 1078872002 1100655274 1126435101 1148168026 9781402058479 1402058470 9781402058462 hd. bd.) 1402058462 hd. bd.) 9786611067243 6611067248 1281067245 9781281067241 10.1007/978-1-4020-5847-9 doi AU@ 000043375115 DEBSZ 442811195 NZ1 12056822 NZ1 14775062 978-1-4020-5846-2 Springer http://www.springerlink.com GW5XE eng pn GW5XE VPI OCLCA CEF OCLCQ MYPMP OCLCO EBLCP OCLCQ A7U OCLCQ BEDGE OCLCQ OCLCO NUI YNG UAB N$T E7B UBC MNU IDEBK OCLCF YDXCP OCLCO DEBSZ OCLCQ OCLCO OCLCQ VT2 OTZ OCLCQ OCLCO ESU CASUM OCL STF OCLCQ U3W AU@ OCLCQ WYU YOU CANPU NZHMA OCLCO OCLCQ WURST OCLCQ SFB UKAHL OCLCA RC lcco MED 062000 bisacsh HEA 039030 bisacsh MJCL bicssc 616.99/463 22 Metastasis of prostate cancer Richard J. Ablin, Malcolm D. Mason (eds.). Dordrecht Springer 2007 Dordrecht Dordrecht Springer 1 online resource (approximately 380 pages) 1 online resource (approximately 380 pages) Text txt rdacontent computer c rdamedia online resource cr rdacarrier Cancer Metastasis - Biology and Treatment 1568-2102 10 Includes bibliographical references and index 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; -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 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 English Prostate- Cáncer- Research Metástasis- Diagnosis Metástasis- Research- Methodology Neoplasm Metastasis Prostatic Neoplasms MEDICAL- Oncology. HEALTH & FITNESS- Diseases- Cáncer Biomédecine. Sciences de la vie. Prostate- Cáncer- Research. neoplasms biomedische wetenschappen biomedicine Medicine (General) Geneeskunde (algemeen) Electronic books Ablin, Richard J. 1940-) Mason, Malcolm Malcolm D.) Print version Metastasis of prostate cancer. Dordrecht : Springer, 2007 9781402058462 1402058462 (OCoLC)123434547 Cancer metastasis (Series) 10. 1568-2102