Tumour-infiltrating regulatory T cells stimulate mammary cancer metastasis through RANKL–RANK signalling
Wei Tan,
Weizhou Zhang,
Amy Strasner,
Sergei Grivennikov,
Jin Q. Cheng,
Robert M. Hoffman and
Michael Karin ()
Additional contact information
Wei Tan: Laboratory of Gene Regulation and Signal Transduction, University of California San Diego School of Medicine, 9500 Gilman Drive, Mail Code 0723, La Jolla, California 92093, USA
Weizhou Zhang: Laboratory of Gene Regulation and Signal Transduction, University of California San Diego School of Medicine, 9500 Gilman Drive, Mail Code 0723, La Jolla, California 92093, USA
Amy Strasner: Laboratory of Gene Regulation and Signal Transduction, University of California San Diego School of Medicine, 9500 Gilman Drive, Mail Code 0723, La Jolla, California 92093, USA
Sergei Grivennikov: Laboratory of Gene Regulation and Signal Transduction, University of California San Diego School of Medicine, 9500 Gilman Drive, Mail Code 0723, La Jolla, California 92093, USA
Jin Q. Cheng: H. Lee Moffitt Cancer Center
Robert M. Hoffman: University of California San Diego
Michael Karin: Laboratory of Gene Regulation and Signal Transduction, University of California San Diego School of Medicine, 9500 Gilman Drive, Mail Code 0723, La Jolla, California 92093, USA
Nature, 2011, vol. 470, issue 7335, 548-553
Abstract:
Metastasis in breast cancer In a mouse model of ErbB-driven mammary tumours, Tan et al. find a role for RANKL (receptor activator of nuclear factor-κB ligand) in the formation of lung metastases. RANKL is produced by regulatory T cells infiltrating the primary tumours, and acts through its receptor RANK, which is expressed on the cancer cells. Targeting RANKL may therefore prove useful in reducing breast cancer metastases.
Date: 2011
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DOI: 10.1038/nature09707
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