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Clin Cancer Res. 2015 Aug 15;21(16):3597-601. doi: 10.1158/1078-0432.CCR-14-2520. Epub 2015 Jun 26.

Molecular Pathways: Activating T Cells after Cancer Cell Phagocytosis from Blockade of CD47 "Don't Eat Me" Signals.

Author information

1
Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California. Ludwig Center for Cancer Stem Cell Research and Medicine, Stanford University School of Medicine, Stanford, California. Stanford Cancer Institute, Stanford University School of Medicine, Stanford, California.
2
Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California. Ludwig Center for Cancer Stem Cell Research and Medicine, Stanford University School of Medicine, Stanford, California. Stanford Cancer Institute, Stanford University School of Medicine, Stanford, California. Institute of Biomedical Studies, Baylor University, Waco, Texas.
3
Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California. Ludwig Center for Cancer Stem Cell Research and Medicine, Stanford University School of Medicine, Stanford, California. Stanford Cancer Institute, Stanford University School of Medicine, Stanford, California. Department of Pathology, Stanford University Medical Center, Stanford, California. irv@stanford.edu.

Abstract

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-α 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-α engagement are attractive therapeutic targets as a monotherapy or in combination with additional immune-modulating agents for activating antitumor T cells in vivo.

PMID:
26116271
PMCID:
PMC4621226
DOI:
10.1158/1078-0432.CCR-14-2520
[Indexed for MEDLINE]
Free PMC Article

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