Skip Navigation


Carcinogenesis Advance Access originally published online on July 16, 2008
Carcinogenesis 2008 29(9):1675-1684; doi:10.1093/carcin/bgn171
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
29/9/1675    most recent
bgn171v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Ager, E. I.
Right arrow Articles by Christophi, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ager, E. I.
Right arrow Articles by Christophi, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

The renin–angiotensin system and malignancy

Eleanor I. Ager*, Jaclyn Neo and Christopher Christophi

Department of Surgery, Austin Health, University of Melbourne, Heidelberg, Victoria 3084, Australia

* To whom correspondence should be addressed. Tel: +61 3 9456 5734; Fax: +61 3 9458 1650; Email: eager{at}unimelb.edu.au

The renin–angiotensin system (RAS) is usually associated with its systemic action on cardiovascular homoeostasis. However, recent studies suggest that at a local tissue level, the RAS influences tumour growth. The potential of the RAS as a target for cancer treatment and the suggested underlying mechanisms of its paracrine effects are reviewed here. These include modulation of angiogenesis, cellular proliferation, immune responses and extracellular matrix formation. Knowledge of the RAS has increased dramatically in recent years with the discovery of new enzymes, peptides and feedback mechanisms. The local RAS appears to influence tumour growth and metastases and there is evidence of tissue- and tumour-specific differences. Recent experimental studies provide strong evidence that drugs that inhibit the RAS have the potential to reduce cancer risk or retard tumour growth and metastases. Manipulation of the RAS may, therefore, provide a safe and inexpensive anticancer strategy.

Abbreviations: ACE, ANG I converting enzyme; ANG, Angiotensin; AT1R, Angiotensin II type 1 receptor; AT2R, Angiotensin II type 2 receptor; EMT, epithelial to mesenchymal transition; ET-1, endothelin-1; HSCs, hepatic stellate cells; MasR, mitochondrial assembly receptor; MCP, macrophage/monocyte chemoattractant protein; PDGF, platelet-derived growth factor; RAS, renin-angiotensin system; VEGF, vascular endothelial growth factor

Received April 23, 2008; revised July 10, 2008; accepted July 10, 2008.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 DiabetesHome page
X. Yang, H. Zhao, Y. Sui, R. C.W. Ma, W. Y. So, G. T.C. Ko, A. P.S. Kong, R. Ozaki, C. Y. Yeung, G. Xu, et al.
Additive Interaction Between the Renin-Angiotensin System and Lipid Metabolism for Cancer in Type 2 Diabetes
Diabetes, July 1, 2009; 58(7): 1518 - 1525.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.