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  • Sir Peter MacCallum Department of Oncology
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    Cancer-associated fibroblast-secreted CXCL16 attracts monocytes to promote stroma activation in triple-negative breast cancers

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    56
    Author
    Allaoui, R; Bergenfelz, C; Mohlin, S; Hagerling, C; Salari, K; Werb, Z; Anderson, RL; Ethier, SP; Jirstrom, K; Pahlman, S; ...
    Date
    2016-10-11
    Source Title
    Nature Communications
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Anderson, Robin
    Affiliation
    Sir Peter MacCallum Department of Oncology
    Metadata
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    Document Type
    Journal Article
    Citations
    Allaoui, R., Bergenfelz, C., Mohlin, S., Hagerling, C., Salari, K., Werb, Z., Anderson, R. L., Ethier, S. P., Jirstrom, K., Pahlman, S., Bexell, D., Tahin, B., Johansson, M. E., Larsson, C. & Leandersson, K. (2016). Cancer-associated fibroblast-secreted CXCL16 attracts monocytes to promote stroma activation in triple-negative breast cancers. NATURE COMMUNICATIONS, 7 (1), https://doi.org/10.1038/ncomms13050.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/260309
    DOI
    10.1038/ncomms13050
    Abstract
    Triple-negative (TN) breast cancers (ER-PR-HER2-) are highly metastatic and associated with poor prognosis. Within this subtype, invasive, stroma-rich tumours with infiltration of inflammatory cells are even more aggressive. The effect of myeloid cells on reactive stroma formation in TN breast cancer is largely unknown. Here, we show that primary human monocytes have a survival advantage, proliferate in vivo and develop into immunosuppressive myeloid cells expressing the myeloid-derived suppressor cell marker S100A9 only in a TN breast cancer environment. This results in activation of cancer-associated fibroblasts and expression of CXCL16, which we show to be a monocyte chemoattractant. We propose that this migratory feedback loop amplifies the formation of a reactive stroma, contributing to the aggressive phenotype of TN breast tumours. These insights could help select more suitable therapies targeting the stromal component of these tumours, and could aid prediction of drug resistance.

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