Journal
CELL
Volume 141, Issue 1, Pages 178-190Publisher
CELL PRESS
DOI: 10.1016/j.cell.2010.02.039
Keywords
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Categories
Funding
- TG
- Methusalem funding
- NCCR Molecular Oncology
- Swiss Science Foundation
- FWO [G. 0229.04, G. 0500.08, SCIE2006-3, OT/08/ 37]
- NIH [CA69184, EY017164]
- Swiss Science Foundation [3100A0108207]
- DFG
- DKH
- [IUAP06/30]
- [GOA2006/11]
- [LSHG-CT-2004-503573]
- [LSHC-CT-2005-518178]
- [SAF 2007-63069]
- [2009 SGR 1496]
- NATIONAL CANCER INSTITUTE [R01CA069184] Funding Source: NIH RePORTER
- NATIONAL EYE INSTITUTE [R01EY017164] Funding Source: NIH RePORTER
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Our findings that PlGF is a cancer target and anti-PlGF is useful for anticancer treatment have been challenged by Bais et al. Here we take advantage of carcinogen-induced and transgenic tumor models as well as ocular neovascularization to report further evidence in support of our original findings of PlGF as a promising target for anticancer therapies. We present evidence for the efficacy of additional anti-PlGF antibodies and their ability to phenocopy genetic deficiency or silencing of PlGF in cancer and ocular disease but also show that not all anti-PlGF antibodies are effective. We also provide additional evidence for the specificity of our anti-PlGF antibody and experiments to suggest that anti-PlGF treatment will not be effective for all tumors and why. Further, we show that PlGF blockage inhibits vessel abnormalization rather than density in certain tumors while enhancing VEGF-targeted inhibition in ocular disease. Our findings warrant further testing of anti-PlGF therapies.
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