Journal
BIOMARKER RESEARCH
Volume 5, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s40364-017-0105-8
Keywords
Unfolded protein response; CD47; Thrombospondin-1; GRP78; Tamoxifen; Endocrine therapy resistance; Innate anti-tumor immunity; Immunometabolism
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Funding
- National Cancer Institute (USA) Career Transition Award [1K22CA181274-01A1]
- Wake Forest Clinical and Translational Science Institute (WF CTSI)
- National Center for Advancing Translational Sciences (NCATS), National Institutes of Health [UL1TR001420]
- Wake Forest Baptist Comprehensive Cancer Center's NCI Cancer Center Support Grant [P30CA012197]
- Chronic Disease Research Fund
- American Cancer Society Research Scholar grant [RSG-16-204-01-NEC]
- Prevent Cancer Foundation
- Comprehensive Cancer Center of Wake Forest Baptist Medical Center, NCI CCSG grant [P30CA012197]
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We recently demonstrated that targeting the unfolded protein response (UPR) protein GRP78 down-regulates CD47 expression, resulting in increased tumor macrophage infiltration and inhibited resistance to anti-estrogen therapy. We now show new data indicating that anti-estrogen therapy regulates CD47 expression and implicates its ligand, thrombospondin-1, in regulation of tumor macrophage infiltration. Moreover, GRP78 and CD47 co-expression is associated with poor prognosis in breast cancer patients, suggesting the existence of crosstalk between UPR and immunity that regulates therapeutic responses in breast cancer.
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