期刊
CANCER CELL
卷 14, 期 3, 页码 263-273出版社
CELL PRESS
DOI: 10.1016/j.ccr.2008.08.001
关键词
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资金
- US National Institutes of Health (NIH) [CA-41233]
- Breast Cancer Research Foundation
- National Cancer Institute of Canada
- Canadian Institutes of Health Research
- Ontario Institute for Cancer Research
- Associazione Italiana per la Ricerca sul Cancro
- Istituto Superione di Sanita
- Sixth EU Framework
- Dr. Saal van Zwanenberg Stichting
- ImClone Systems Inc.
Several 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-1 alpha 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.
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