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Refractoriness to Antivascular Endothelial Growth Factor Treatment: Role of Myeloid Cells

Genentech, Inc., South San Francisco, California

Requests for reprints: Napoleone Ferrara, Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080. Phone: 650-225 2968; Fax: 650-225 4265; E-mail: nf{at}gene.com.

Key Words: angiogenesis • VEGF • tumor • stroma • CD11b+Gr1+ Cells

CD11b+Gr1+ cells, which include neutrophils, macrophages, and myeloid-derived suppressor cells, have been shown to contribute to tumor angiogenesis. Recently, we found that accumulation of CD11b+Gr1+ in tumors renders them refractory to angiogenic blockade by vascular endothelial growth factor (VEGF) antibodies. This effect was traced to a pathway of CD11b+Gr1+–mediated angiogenesis that is, at least in part, driven by the secreted protein Bv8, which is up-regulated by the important myeloid growth factor granulocyte colony-stimulating factor (G-CSF). Thus, G-CSF may promote tumor angiogenesis through a Bv8-dependent pathway that bypasses VEGF and renders tumors refractory to anti-VEGF therapy. [Cancer Res 2008;68(14):5501–4]

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