Journal article
Loss of Host Type-I IFN Signaling Accelerates Metastasis and Impairs NK-cell Antitumor Function in Multiple Models of Breast Cancer
J Rautela, N Baschuk, CY Slaney, KM Jayatilleke, K Xiao, BN Bidwell, EC Lucas, ED Hawkins, P Lock, CS Wong, W Chen, RL Anderson, PJ Hertzog, DM Andrews, A Möller, BS Parker
Cancer Immunology Research | Published : 2015
Abstract
Metastatic progression is the major cause of breast cancer related mortality. By examining multiple syngeneic preclinical breast cancer models in mice lacking a functional type-I interferon receptor (Ifnar1-/- mice), we show that host-derived type-I interferon (IFN) signaling is a critical determinant of metastatic spread that is independent of primary tumor growth. In particular, we show that bone metastasis can be accelerated in Balb/c Ifnar1-/- mice bearing either 4T1 or 66cl4 orthotopic tumors and, for the first time, present data showing the development of bone metastasis in the C57Bl/6 spontaneous MMTV-PyMTdriven model of tumorigenesis. Further exploration of these results revealed tha..
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Funding Acknowledgements
This work was supported by grant funding from the Cancer Council Victoria (to B.S. Parker and P.J. Hertzog), the National Health and Medical Research Council (NHMRC; to B.S. Parker and P.J. Hertzog), fellowship support from NHMRC and ARC (to B.S. Parker and P.J. Hertzog), and the National Breast Cancer Foundation [NBCF; fellowships to CYS (co-funded by Cure Cancer Australia), R.L. Anderson, and A. Moller].