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Cancer Immunol Res. 2015 Aug;3(8):849-54. doi: 10.1158/2326-6066.CIR-15-0100. Epub 2015 Jun 29.

Ablation of B7-H3 but Not B7-H4 Results in Highly Increased Tumor Burden in a Murine Model of Spontaneous Prostate Cancer.

Author information

1
Program in Immunology, Howard Hughes Medical Institute, and Ludwig Center for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center, New York, New York.
2
Columbia University Medical Center, New York, New York. Centre of Allergy and Environment (ZAUM), Technical University and Helmholtz Centre Munich, Munich, Germany.
3
Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York. Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York.
4
Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
5
Department of Pathology, University of Chicago, Chicago, Illinois.
6
Department of Immunology and Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.
7
Program in Immunology, Howard Hughes Medical Institute, and Ludwig Center for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center, New York, New York. Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas. JAllison@mdanderson.org.

Abstract

The costimulatory molecules B7-H3 and B7-H4 are overexpressed in a variety of human tumors and have been hypothesized as possible biomarkers and immunotherapeutic targets. Despite this potential, the predominating uncertainty about their functional implication in tumor-host interaction hampers their evaluation as a target for cancer therapy. By means of a highly physiologic, spontaneous tumor model in mice, we establish a causal link between B7-H3 and host tumor control and found B7-H4 to be redundant.

PMID:
26122284
PMCID:
PMC5939565
DOI:
10.1158/2326-6066.CIR-15-0100
[Indexed for MEDLINE]
Free PMC Article

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