Cessation of CCL2 inhibition accelerates breast cancer metastasis by promoting angiogenesis

Laura Bonapace, Marie-May Coissieux, Jeffrey Wyckoff, Kirsten D. Mertz, Zsuzsanna Varga, Tobias Junt and Mohamed Bentires-Alj ()
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Laura Bonapace: Friedrich Miescher Institute for Biomedical Research (FMI), Basel 4058, 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
Kirsten D. Mertz: University Hospital Zurich, 8006 Zurich, 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

Nature, 2014, vol. 515, issue 7525, 130-133

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.

Date: 2014
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DOI: 10.1038/nature13862

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