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Antiangiogenic Strategies on Defense: On the Possibility of Blocking Rebounds by the Tumor Vasculature after Chemotherapy

Sunnybrook Health Sciences Centre, Molecular and Cellular Biology Research, and Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada

Requests for reprints: Robert S. Kerbel, Sunnybrook and Women's College Health Sciences Centre, S-217 Research Building, 2075 Bayview Avenue, Toronto, Ontario, Canada M4N 3M5. Phone: 416-480-5711; Fax: 416-480-5884; E-mail: Cassandra.Cheng{at}swri.ca.

Rapid or accelerated tumor cell repopulation after significant tumor cell killing induced by various cytotoxic agents often compromises the expected therapeutic benefit of such tumor responses. Here, we discuss the concept that tumor cell repopulation after certain cytotoxic therapies, using vascular disrupting agents as an example, may be aided by a reactive, systemic host response involving the mobilization of bone marrow–derived circulating cells, including endothelial progenitor cells, which subsequently home to the vasculature of treated tumors and promote tumor neovascularization. These vasculogenic "rebounds" can be blocked, at least in some cases, by treatment with an antiangiogenic drug. There is limited preliminary evidence that maximum tolerated dose chemotherapy causes a similar effect. This could constitute one way by which antiangiogenic therapy could increase the efficacy of conventional cytotoxic chemotherapy regimens; it also raises the specter of new molecular targets for systemic cancer therapies which are involved in therapy-induced bone marrow–derived cell mobilization, homing to tumors, and tumor retention. [Cancer Res 2007;67(15):7055–8]

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