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Cessation of CCL2 inhibition accelerates breast cancer metastasis by promoting angiogenesis

Author

Listed:
  • Laura Bonapace

    (Friedrich Miescher Institute for Biomedical Research (FMI), Basel 4058, Switzerland
    Novartis Institutes for Biomedical Research, 4002 Basel, Switzerland)

  • Marie-May Coissieux

    (Friedrich Miescher Institute for Biomedical Research (FMI), Basel 4058, Switzerland)

  • Jeffrey Wyckoff

    (Friedrich Miescher Institute for Biomedical Research (FMI), Basel 4058, Switzerland
    Present address: Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.)

  • Kirsten D. Mertz

    (University Hospital Zurich, 8006 Zurich, Switzerland
    Institute of Pathology Liestal, Cantonal Hospital Baselland, 4410 Liestal, Switzerland)

  • Zsuzsanna Varga

    (University Hospital Zurich, 8006 Zurich, Switzerland)

  • Tobias Junt

    (Novartis Institutes for Biomedical Research, 4002 Basel, Switzerland)

  • Mohamed Bentires-Alj

    (Friedrich Miescher Institute for Biomedical Research (FMI), Basel 4058, Switzerland)

Abstract

In mouse models of breast cancer, anti-CCL2 therapy—thought to be potentially useful in treating cancer—is shown to accelerate the growth of lung metastases on discontinuation due to a surge of recruitment of bone marrow monocytes and increased interleukin-6-dependent vascularization of the lung metastatic environment.

Suggested Citation

  • Laura Bonapace & Marie-May Coissieux & Jeffrey Wyckoff & Kirsten D. Mertz & Zsuzsanna Varga & Tobias Junt & Mohamed Bentires-Alj, 2014. "Cessation of CCL2 inhibition accelerates breast cancer metastasis by promoting angiogenesis," Nature, Nature, vol. 515(7525), pages 130-133, November.
    • Handle: RePEc:nat:nature:v:515:y:2014:i:7525:d:10.1038_nature13862
    DOI: 10.1038/nature13862
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