Author/Authors :
Shaked، نويسنده , , Yuval and Henke، نويسنده , , Erik and Roodhart، نويسنده , , Jeanine M.L. and Mancuso، نويسنده , , Patrizia and Langenberg، نويسنده , , Marlies H.G. and Colleoni، نويسنده , , Marco and Daenen، نويسنده , , Laura G. and Man، نويسنده , , Shan and Xu، نويسنده , , Ping and Emmenegger، نويسنده , , Urban and Tang، نويسنده , , Terence and Zhu، نويسنده , , Zhenping and Witte، نويسنده , , Larry and Strieter، نويسنده , , Robert M. and Bertolini، نويسنده , , Francesco and Voest، نويسنده , , Emile E. and Benezra، نويسنده , , Robert S. Kerbel، نويسنده , , Robert S.، نويسنده ,
Abstract :
Summary
l hypotheses have been proposed to explain how antiangiogenic drugs enhance the treatment efficacy of cytotoxic chemotherapy, including impairing the ability of chemotherapy-responsive tumors to regrow after therapy. With respect to the latter, we show that certain chemotherapy drugs, e.g., paclitaxel, can rapidly induce proangiogenic bone marrow-derived circulating endothelial progenitor (CEP) mobilization and subsequent tumor homing, whereas others, e.g., gemcitabine, do not. Acute CEP mobilization was mediated, at least in part, by systemic induction of SDF-1α and could be prevented by various procedures such as treatment with anti-VEGFR2 blocking antibodies or paclitaxel treatment in CEP-deficient Id mutant mice, both of which resulted in enhanced antitumor effects mediated by paclitaxel, but not by gemcitabine.
