CCL2 recruits inflammatory monocytes to facilitate breast-tumour metastasis

Bin-Zhi Qian, Jiufeng Li, Hui Zhang, Takanori Kitamura, Jinghang Zhang, Liam R. Campion, Elizabeth A. Kaiser, Linda A. Snyder and Jeffrey W. Pollard ()
Additional contact information
Bin-Zhi Qian: Center for the Study of Reproductive Biology and Women’s Health, Albert Einstein College of Medicine
Jiufeng Li: Center for the Study of Reproductive Biology and Women’s Health, Albert Einstein College of Medicine
Hui Zhang: Center for the Study of Reproductive Biology and Women’s Health, Albert Einstein College of Medicine
Takanori Kitamura: Center for the Study of Reproductive Biology and Women’s Health, Albert Einstein College of Medicine
Jinghang Zhang: Flow Cytometry Core Facility, Albert Einstein College of Medicine
Liam R. Campion: Ortho Biotech Oncology R&D, 145 King of Prussia Road
Elizabeth A. Kaiser: Ortho Biotech Oncology R&D, 145 King of Prussia Road
Linda A. Snyder: Ortho Biotech Oncology R&D, 145 King of Prussia Road
Jeffrey W. Pollard: Center for the Study of Reproductive Biology and Women’s Health, Albert Einstein College of Medicine

Nature, 2011, vol. 475, issue 7355, 222-225

Abstract: Monocyte recruitment in metastasis Macrophages are abundant in tumours, where they promote tumorigenesis and metastasis. Jeffrey Pollard and colleagues now identify inflammatory monocytes as a precursor population for the macrophages that promote breast cancer metastasis to the lung or bone. These cells are recruited through the cytokine CCL2 and promote tumour-cell extravasation (by producing the signal protein VEGF) and the seeding of metastases. These findings can explain the poor prognosis for breast cancer patients with elevated expression of CCL2.

Date: 2011
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DOI: 10.1038/nature10138

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