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PlGF Blockade Does Not Inhibit Angiogenesis during Primary Tumor Growth
Author(s) -
Carlos Bais,
Xiumin Wu,
Jenny Yao,
Suya Yang,
Yongping Crawford,
Krista McCutcheon,
Christine Tan,
Ganesh Kolumam,
Jean-Michel Vernes,
Jeffrey EasthamAnderson,
Peter C. Haughney,
Marcin Kowanetz,
Thijs J. Hagenbeek,
Ian Kasman,
Hani Bou Reslan,
Jed Ross,
Nick van Bruggen,
Richard A.D. Carano,
Yu-Ju Gloria Meng,
Jo-Anne Hongo,
Jean Philippe Stephan,
Masabumi Shibuya,
Napoleone Ferrara
Publication year - 2010
Publication title -
cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 26.304
H-Index - 776
eISSN - 1097-4172
pISSN - 0092-8674
DOI - 10.1016/j.cell.2010.01.033
Subject(s) - placental growth factor , cancer research , angiogenesis , biology , antibody , blockade , metastasis , extravasation , blocking antibody , tyrosine kinase , receptor tyrosine kinase , vascular endothelial growth factor , cancer , receptor , vegf receptors , immunology , biochemistry , genetics
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.

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