4.8 Article

Further Pharmacological and Genetic Evidence for the Efficacy of PlGF Inhibition in Cancer and Eye Disease

期刊

CELL
卷 141, 期 1, 页码 178-190

出版社

CELL PRESS
DOI: 10.1016/j.cell.2010.02.039

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资金

  1. TG
  2. Methusalem funding
  3. NCCR Molecular Oncology
  4. Swiss Science Foundation
  5. FWO [G. 0229.04, G. 0500.08, SCIE2006-3, OT/08/ 37]
  6. NIH [CA69184, EY017164]
  7. Swiss Science Foundation [3100A0108207]
  8. DFG
  9. DKH
  10. [IUAP06/30]
  11. [GOA2006/11]
  12. [LSHG-CT-2004-503573]
  13. [LSHC-CT-2005-518178]
  14. [SAF 2007-63069]
  15. [2009 SGR 1496]
  16. NATIONAL CANCER INSTITUTE [R01CA069184] Funding Source: NIH RePORTER
  17. NATIONAL EYE INSTITUTE [R01EY017164] Funding Source: NIH RePORTER

向作者/读者索取更多资源

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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