Metastasis of Prostate Cancer

  • Richard J. Ablin
  • Malcolm D. Mason

Part of the Cancer Metastasis – Biology and Treatment book series (CMBT, volume 10)

Table of contents

  1. Front Matter
    Pages I-XIV
  2. Richard J. Ablin, Malcolm D. Mason
    Pages 1-3
  3. David F. Penson, Peter C. Albertsen
    Pages 5-19
  4. Ruchi M. Newman, Bruce R. Zetter
    Pages 111-125
  5. Mary J.C. Hendrix, Jun Luo, Elisabeth A. Seftor, Navesh Sharma, Paul M. Heidger Jr., Michael B. Cohen et al.
    Pages 127-141
  6. Gaynor Davies, Gregory M. Harrison, Malcolm D. Mason
    Pages 171-196
  7. Gaynor Davies, Wen G. Jiang, Malcolm D. Mason
    Pages 197-219
  8. Michael J. Wilson, Akhouri A. Sinha
    Pages 221-251
  9. Mike Shelley, Charles L. Bennett, Derek Nathan, Oliver Sartor
    Pages 283-307
  10. Paula Scullin, Joe M. O’Sullivan, Christopher C. Parker
    Pages 309-335
  11. Takefumi Satoh, Terry L. Timme, Yehoshua Gdor, Brian J. Miles, Robert J. Amato, Dov Kadmon et al.
    Pages 337-353
  12. Richard J. Ablin, Malcolm D. Mason
    Pages 355-397
  13. Back Matter
    Pages 399-407

About this book

Introduction

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.

Keywords

bisphosphonates cell chemotherapy drug design gene therapy metastasis molecular biology prostate cancer radiotherapy tumor

Editors and affiliations

  • Richard J. Ablin
    • 1
  • Malcolm D. Mason
    • 2
  1. 1.University of Arizona College of Medicine, and the Arizona Cancer CenterTucsonU.S.A
  2. 2.University of CardiffU.K

Bibliographic information

  • DOI https://doi.org/10.1007/978-1-4020-5847-9
  • Copyright Information Springer Science+Business Media B.V. 2007
  • Publisher Name Springer, Dordrecht
  • eBook Packages Biomedical and Life Sciences
  • Print ISBN 978-1-4020-5846-2
  • Online ISBN 978-1-4020-5847-9
  • Series Print ISSN 1568-2102
  • About this book