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. © 2010 Elsevier Inc.

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

Dettori D.;Mazzone M.;
2010-01-01

Abstract

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. © 2010 Elsevier Inc.
2010
141
1
178
190
Cellcylce; Cellimunno; Humdisease; Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Carcinoma, Hepatocellular; Choroid; Disease Models, Animal; Eye Diseases; Humans; Liver Neoplasms, Experimental; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Transgenic; Neovascularization, Physiologic; Papilloma; Placenta Growth Factor; Pregnancy Proteins; Skin Neoplasms
Van de Veire S.; Stalmans I.; Heindryckx F.; Oura H.; Tijeras-Raballand A.; Schmidt T.; Loges S.; Albrecht I.; Jonckx B.; Vinckier S.; Van Steenkiste C.; Tugues S.; Rolny C.; De Mol M.; Dettori D.; Hainaud P.; Coenegrachts L.; Contreres J.-O.; Van Bergen T.; Cuervo H.; Xiao W.-H.; Le Henaff C.; Buysschaert I.; Masouleh B.K.; Geerts A.; Schomber T.; Bonnin P.; Lambert V.; Haustraete J.; Zacchigna S.; Rakic J.-M.; Jimenez W.; Noel A.; Giacca M.; Colle I.; Foidart J.-M.; Tobelem G.; Morales-Ruiz M.; Vilar J.; Maxwell P.; Vinores S.A.; Carmeliet G.; Dewerchin M.; Claesson-Welsh L.; Dupuy E.; Van Vlierberghe H.; Christofori G.; Mazzone M.; Detmar M.; Collen D.; Carmeliet P.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1841138
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