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.

Further pharmacological and genetic evidence for the efficacy of PlGF inhibition in cancer and eye disease / S. V., D.e., I., S., F., H., H., O., A., T.R., T., S., S., L., I., A., B., J., S., V., C. V., S., S., T., C., R., M. D., M., D., D., P., H., L., C., J., C., T. V., B., H., C., et al.. - In: CELL. - ISSN 0092-8674. - ELETTRONICO. - 141:(2010), pp. 178-190. [10.1016/j.cell.2010.02.039]

Further pharmacological and genetic evidence for the efficacy of PlGF inhibition in cancer and eye disease.

ZACCHIGNA, SERENA;GIACCA, MAURO;
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.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11368/2493557
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