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Tie2-Expressing Monocytes and Tumor Angiogenesis: Regulation by Hypoxia and Angiopoietin-2

¹ Tumor Targeting Group, Academic Unit of Pathology, The Sir Henry Wellcome Laboratories for Medical Research, University of Sheffield Medical School, Sheffield, United Kingdom; ² Angiogenesis and Tumor Targeting Research Unit, and San Raffaele Telethon Institute for Gene Therapy, San Raffaele Scientific Institute; and ³ San Raffaele Vita-Salute University, Milan, Italy

Requests for reprints: Claire E. Lewis, Tumor Targeting Group, Academic Unit of Pathology, The Sir Henry Wellcome Laboratories for Medical Research, University of Sheffield Medical School, Sheffield S10 2RX, United Kingdom. Phone: 44-114-271-2903; Fax: 44-114-271-2903; E-mail: claire.lewis{at}sheffield.ac.uk.

Recent findings indicate that tumor-associated macrophages are important drivers of tumor angiogenesis. Here, we review the essential role played by Tie2-expressing monocytes (TEM) in this phenomenon. TEMs are present in human blood and tumors and their elimination in various tumor models suppresses tumor angiogenesis. A ligand for Tie2, angiopoietin-2 (Ang-2), is produced by angiogenic tumor vessels and is a chemoattractant for TEMs. Hypoxia up-regulates Tie2 expression on TEMs and, together with Ang-2, down-regulates their antitumor functions. Learning more about the regulation of TEMs by the tumor microenvironment may yield new strategies to ablate the tumor vasculature. [Cancer Res 2007;67(18):8429–32]

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