Abstract
This chapter summarizes preclinical data that demonstrated that receptor activator of the nuclear factor kB ligand (RANKL) is essential for osteoclast formation, function, and survival. Furthermore, there is substantial evidence that tumor cell-mediated osteolysis occurs predominantly via induction of RANKL within the bone stroma. The observations that inhibition of RANKL in animal models of bone metastasis blocks tumor-induced osteolysis and prevents the establishment and progression of bony tumors provides the basic rationale for the development of a RANKL inhibitor and application in clinical trials for the treatment and prevention of skeletal related events (SREs). Denosumab, a fully human monoclonal antibody with high affinity and specificity for RANKL, inhibits osteoclast function and bone resorption by binding and neutralizing RANKL. Currently, large clinical studies are ongoing to provide a more precise estimate of the effect of denosumab treatment on the risk of SREs in cancer patients.
Published Version
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