期刊
CLINICAL CANCER RESEARCH
卷 21, 期 16, 页码 3597-3601出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1078-0432.CCR-14-2520
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资金
- PHS grant - NCI, U.S. Department of Health and Human Services [T32 CA09151]
- Institute of Biomedical Studies Fellowship at Baylor University
- NCI
- National Heart, Lung, and Blood Institute of the NIH [R01CA086017, P01CA139490, R01HL058770]
- California Institute for Regenerative Medicine [DR1-01485, DR3-06965]
- Virginia and D.K. Ludwig Fund for Cancer Research
- Joseph & Laurie Lacob Gynecologic/Ovarian Cancer Fund
Recent advances with immunotherapy agents for the treatment of cancer have provided remarkable, and in some cases, curative results. Our laboratory has identified CD47 as an important don't eat me signal expressed on malignant cells. Blockade of the CD47: SIRP-a axis between tumor cells and innate immune cells (monocytes, macrophages, and dendritic cells) increases tumor cell phagocytosis in both solid tumors (including, but not limited to, bladder, breast, colon, lung, and pancreatic) and hematologic malignancies. These phagocytic innate cells are also professional antigen-presenting cells (APC), providing a link from innate to adaptive antitumor immunity. Preliminary studies have demonstrated that APCs present antigens from phagocytosed tumor cells, causing T-cell activation. Therefore, agents that block the CD47: SIRP-a engagement are attractive therapeutic targets as a monotherapy or in combination with additional immune-modulating agents for activating antitumor T cells in vivo. (C) 2015 AACR.
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