Anti-PlGF inhibits growth of VEGF(R)-inhibitor-resistant tumors without affecting healthy vessels.
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Anti-PlGF inhibits growth of VEGF(R)-inhibitor-resistant tumors without affecting healthy vessels. / Fischer, Christian; Jonckx, Bart; Mazzone, Massimiliano; Zacchigna, Serena; Loges, Sonja; Pattarini, Lucia; Chorianopoulos, Emmanuel; Liesenborghs, Laurens; Koch, Marta; Maria, De Mol; Autiero, Monica; Wyns, Sabine; Plaisance, Stephane; Moons, Lieve; van Rooijen, Nico; Giacca, Mauro; Stassen, Jean-Marie; Dewerchin, Mieke; Collen, Desire; Carmeliet, Peter.
in: CELL, Jahrgang 131, Nr. 3, 3, 2007, S. 463-475.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Anti-PlGF inhibits growth of VEGF(R)-inhibitor-resistant tumors without affecting healthy vessels.
AU - Fischer, Christian
AU - Jonckx, Bart
AU - Mazzone, Massimiliano
AU - Zacchigna, Serena
AU - Loges, Sonja
AU - Pattarini, Lucia
AU - Chorianopoulos, Emmanuel
AU - Liesenborghs, Laurens
AU - Koch, Marta
AU - Maria, De Mol
AU - Autiero, Monica
AU - Wyns, Sabine
AU - Plaisance, Stephane
AU - Moons, Lieve
AU - van Rooijen, Nico
AU - Giacca, Mauro
AU - Stassen, Jean-Marie
AU - Dewerchin, Mieke
AU - Collen, Desire
AU - Carmeliet, Peter
PY - 2007
Y1 - 2007
N2 - Novel antiangiogenic strategies with complementary mechanisms are needed to maximize efficacy and minimize resistance to current angiogenesis inhibitors. We explored the therapeutic potential and mechanisms of alphaPlGF, an antibody against placental growth factor (PlGF), a VEGF homolog, which regulates the angiogenic switch in disease, but not in health. alphaPlGF inhibited growth and metastasis of various tumors, including those resistant to VEGF(R) inhibitors (VEGF(R)Is), and enhanced the efficacy of chemotherapy and VEGF(R)Is. alphaPlGF inhibited angiogenesis, lymphangiogenesis, and tumor cell motility. Distinct from VEGF(R)Is, alphaPlGF prevented infiltration of angiogenic macrophages and severe tumor hypoxia, and thus, did not switch on the angiogenic rescue program responsible for resistance to VEGF(R)Is. Moreover, it did not cause or enhance VEGF(R)I-related side effects. The efficacy and safety of alphaPlGF, its pleiotropic and complementary mechanism to VEGF(R)Is, and the negligible induction of an angiogenic rescue program suggest that alphaPlGF may constitute a novel approach for cancer treatment.
AB - Novel antiangiogenic strategies with complementary mechanisms are needed to maximize efficacy and minimize resistance to current angiogenesis inhibitors. We explored the therapeutic potential and mechanisms of alphaPlGF, an antibody against placental growth factor (PlGF), a VEGF homolog, which regulates the angiogenic switch in disease, but not in health. alphaPlGF inhibited growth and metastasis of various tumors, including those resistant to VEGF(R) inhibitors (VEGF(R)Is), and enhanced the efficacy of chemotherapy and VEGF(R)Is. alphaPlGF inhibited angiogenesis, lymphangiogenesis, and tumor cell motility. Distinct from VEGF(R)Is, alphaPlGF prevented infiltration of angiogenic macrophages and severe tumor hypoxia, and thus, did not switch on the angiogenic rescue program responsible for resistance to VEGF(R)Is. Moreover, it did not cause or enhance VEGF(R)I-related side effects. The efficacy and safety of alphaPlGF, its pleiotropic and complementary mechanism to VEGF(R)Is, and the negligible induction of an angiogenic rescue program suggest that alphaPlGF may constitute a novel approach for cancer treatment.
M3 - SCORING: Zeitschriftenaufsatz
VL - 131
SP - 463
EP - 475
JO - CELL
JF - CELL
SN - 0092-8674
IS - 3
M1 - 3
ER -
