PlGF blockade does not inhibit angiogenesis during primary tumor growth

Cell. 2010 Apr 2;141(1):166-77. doi: 10.1016/j.cell.2010.01.033.


It has been recently reported that treatment with an anti-placenta growth factor (PlGF) antibody inhibits metastasis and primary tumor growth. Here we show that, although anti-PlGF treatment inhibited wound healing, extravasation of B16F10 cells, and growth of a tumor engineered to overexpress the PlGF receptor (VEGFR-1), neutralization of PlGF using four novel blocking antibodies had no significant effect on tumor angiogenesis in 15 models. Also, genetic ablation of the tyrosine kinase domain of VEGFR-1 in the host did not result in growth inhibition of the anti-VEGF-A sensitive or resistant tumors tested. Furthermore, combination of anti-PlGF with anti-VEGF-A antibodies did not result in greater antitumor efficacy than anti-VEGF-A monotherapy. In conclusion, our data argue against an important role of PlGF during primary tumor growth in most models and suggest that clinical evaluation of anti-PlGF antibodies may be challenging.

MeSH terms

  • Animals
  • Antibodies, Monoclonal / pharmacology
  • Cell Line, Tumor
  • Humans
  • Mice
  • Mice, Inbred BALB C
  • Neoplasms / blood supply*
  • Neovascularization, Pathologic*
  • Placenta Growth Factor
  • Pregnancy Proteins / antagonists & inhibitors
  • Pregnancy Proteins / metabolism*
  • Vascular Endothelial Growth Factors


  • Antibodies, Monoclonal
  • PGF protein, human
  • Pgf protein, mouse
  • Pregnancy Proteins
  • Vascular Endothelial Growth Factors
  • Placenta Growth Factor