Sponsor
Elliott S et al. – One of the potential mechanisms proffered to explain the observed safety issues was that functional EpoR was expressed in tumors and/or endothelial cells, and that ESAs directly stimulated tumor growth and/or antagonized tumor ablative therapies. Since then, numerous groups have performed further research evaluating this potential mechanism with conflicting data and conclusions. Here, authors review the biology of endogenous Epo and EpoR expression and function in erythropoiesis, and evaluate the evidence pertaining to the expression of EpoR on normal nonhematopoietic and tumor cells.
Register now to view all the MDLinx contents (FREE)!
Login
Sponsor
Stay current - Media Tool
♦ Subscribe to our free RSS feeds:
Get the latest news in your specialty automatically added to your newsreader or your personal My Yahoo!, Google, My MSN or My AOL page. Learn More ♦
♦ Follow Us on Twitter
Twitter is a rich source of instantly updated information. Join today and follow @MDLinx to start receiving tweets. Learn More ♦
Close
Sponsor