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

Claire E. Lewis, Michele De Palma and Luigi Naldini
Claire E. Lewis
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Michele De Palma
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Luigi Naldini
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DOI: 10.1158/0008-5472.CAN-07-1684 Published September 2007
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Abstract

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]

  • Tie2
  • monocyte
  • Angiopoietin-2
  • hypoxia
  • angiogenesis

Footnotes

    • Received May 8, 2007.
    • Revision received June 19, 2007.
    • Accepted June 19, 2007.
    • ©2007 American Association for Cancer Research.
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    Cancer Research: 67 (18)
    September 2007
    Volume 67, Issue 18
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    Tie2-Expressing Monocytes and Tumor Angiogenesis: Regulation by Hypoxia and Angiopoietin-2
    Claire E. Lewis, Michele De Palma and Luigi Naldini
    Cancer Res September 15 2007 (67) (18) 8429-8432; DOI: 10.1158/0008-5472.CAN-07-1684

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    Tie2-Expressing Monocytes and Tumor Angiogenesis: Regulation by Hypoxia and Angiopoietin-2
    Claire E. Lewis, Michele De Palma and Luigi Naldini
    Cancer Res September 15 2007 (67) (18) 8429-8432; DOI: 10.1158/0008-5472.CAN-07-1684
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    • Article
      • Abstract
      • Bone Marrow–Derived Cells Regulate Tumor Angiogenesis
      • Identification of TEMs
      • Role of TEMs in Tumor Angiogenesis: Insights from Mouse Tumor Models
      • Regulation of TEMs by the Tumor Microenvironment
      • Concluding Remarks
      • Acknowledgments
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