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Wnt Antagonism in Multiple Myeloma: A Potential Cause of Uncoupled Bone Remodeling

Author's Affiliation: Division of Hematology/Oncology, Cornell University Medical College, New York, New York

Requests for reprints: Roger N. Pearse, Division of Hematology/Oncology, Cornell University Medical College, 1300 York Avenue, Box 113, New York, NY 10021. Phone: 212-746-3964; Fax: 212-746-7888; E-mail: rnp2001{at}med.cornell.edu.

Bone disease in patients with multiple myeloma (MM) is characterized by uncoupled bone remodeling, evident as enhanced osteolytic resorption and decreased rather than increased bone formation. MM-triggered osteolysis follows deregulation of the receptor activator of nuclear factor B ligand (RANKL)/osteoprotegerin cytokine axis. Inhibition of bone formation may result from the ability of MM to inhibit the function of Wnts, secreted glycoproteins critical to osteoblast development. Recent studies show how these processes may be linked.

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