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[Cancer Research 61, 3561-3565, May 1, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

Erythropoietin and Erythropoietin Receptor Expression in Human Cancer1

Geza Acs2, Peter Acs2, Susan M. Beckwith, Richard L. Pitts, Emily Clements, Kondi Wong and Ajay Verma3

Department of Pathology and Laboratory Medicine, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104 [G. A.]; Department of Neurology [P. A., S. M. B., R. L. P., E. C., A. V.] and The United States Military Cancer Institute [A. V.], The Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814; and Department of Neuropathology, Armed Forces Institute of Pathology, Washington, DC 20306 [K. W.]

Erythropoietin (EPO) stimulates the growth of erythroblasts in the bone marrow (C. Lacombe and P. Mayeux, Nephrol. Dial. Transplant., 14 (Suppl. 2): 22–28, 1999). We report basal and hypoxia-stimulated expression of EPO and its receptor, EPOR, in human breast cancer cells, and we demonstrate EPO-stimulated tyrosine phosphorylation and the proliferation of these cells in vitro. In 50 clinical specimens of breast carcinoma, we report high levels of EPO and EPOR associated with malignant cells and tumor vasculature but not with normal breast, benign papilloma, or fibrocystic tissue. Hypoxic tumor regions display the highest levels of EPO and EPOR expression. Enhanced EPO signaling may contribute to the promotion of human cancer by tissue hypoxia.




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