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Advances in Treating Metastatic Bone Cancer |
Authors' Affiliations: 1 University of Virginia, Charlottesville, Virginia; 2 Scios, Inc., Fremont, California; 3 University of Washington, Seattle, Washington; and 4 University of Arkansas for Medical Sciences, Little Rock, Arkansas
Requests for reprints: Theresa A. Guise, Division of Endocrinology, Department of Medicine, University of Virginia, Aurbach Medical Research Building, P. O. Box 801419, Charlottesville, VA 22903. Phone: 434-243-9284; E-mail: tag4n{at}virginia.edu.
Certain solid tumors metastasize to bone and cause osteolysis and abnormal new bone formation. The respective phenotypes of dysregulated bone destruction and bone formation represent two ends of a spectrum, and most patients will have evidence of both. The mechanisms responsible for tumor growth in bone are complex and involve tumor stimulation of the osteoclast and the osteoblast as well as the response of the bone microenvironment. Furthermore, factors that increase bone resorption, independent of tumor, such as sex steroid deficiency, may contribute to this vicious cycle of tumor growth in bone. This article discusses mechanisms and therapeutic implications of osteolytic and osteoblastic bone metastases.
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