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A Causal Role for Endothelin-1 in the Pathogenesis of Osteoblastic Bone Metastases

Yin, Khalid S. Mohammad, Sanna M. Käkönen, Stephen Harris, J. Ruth Wu-Wong, Jerry L. Wessale, Robert J. Padley, I. Ross Garrett, John M. Chirgwin and Theresa A. Guise
Proceedings of the National Academy of Sciences of the United States of America
Vol. 100, No. 19 (Sep. 16, 2003), pp. 10954-10959
Stable URL: http://www.jstor.org/stable/3147411
Page Count: 6
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
A Causal Role for Endothelin-1 in the Pathogenesis of Osteoblastic Bone Metastases
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Abstract

Osteoblastic bone metastases are common in prostate and breast cancer patients, but mechanisms by which tumor cells stimulate new bone formation are unclear. We identified three breast cancer cell lines that cause osteoblastic metastases in a mouse model and secrete endothelin-1. Tumor-produced endothelin-1 stimulates new bone formation in vitro and osteoblastic metastases in vivo via the endothelin A receptor. Treatment with an orally active endothelin A receptor antagonist dramatically decreased bone metastases and tumor burden in mice inoculated with ZR-75-1 cells. Tumor-produced endothelin-1 may have a major role in the establishment of osteoblastic bone metastases, and endothelin A receptor blockade represents effective treatment.

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