Journal article
CD73-Deficient mice are resistant to carcinogenesis
J Stagg, PA Beavis, U Divisekera, MCP Liu, A Möller, PK Darcy, MJ Smyth
Cancer Research | AMER ASSOC CANCER RESEARCH | Published : 2012
Abstract
CD73 is a cell surface 5′-nucleotidase that converts AMP to adenosine, an immune suppressive molecule. CD73 may promote immune escape in cancer by contributing to the degradation of extracellular ATP released by dying cancer cells in hypoxic tumors or following chemotherapy. However, whether CD73 exerts a critical oncogenic function during tumorigenesis is unknown. In this study, we used genetically deficient mice to investigate its contribution to autochthonous tumor formation. CD73 deficiency suppressed the development of 3-methylcholanthrene (MCA)-induced fibrosarcomas through a mechanism relying upon IFN-γ, natural killer (NK) cells, and CD8 + T cells. Similarly, CD73 deficiency also sup..
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Grants
Awarded by National Health and Medical Research Council of Australia
Awarded by Victorian Cancer Agency
Awarded by NH&MRC Australia Fellowship
Funding Acknowledgements
This work was supported by the National Health and Medical Research Council of Australia (1013667), the Prostate Cancer Foundation of Australia, the Association of International Cancer Research, the Victorian Cancer Agency (EOI09_71), and the Canadian Institutes of Health Research. M.J. Smyth was supported by a NH&MRC Australia Fellowship (628623), J. Stagg was supported by the Famille Sabourin Research Chair of University of Montreal, P.K. Darcy was supported by a NH&MRC CDF award, and A. Moller was supported by a NBCF fellowship.