Abstract
Bone destruction is mediated by osteoclasts, whose formation, function, and survival requires the receptor activator of NF-kB ligand (RANKL). Denosumab is a fully human monoclonal antibody to RANKL, thereby inhibiting osteoclast-mediated bone destruction, and blocks the vicious cycle of cancer-mediated bone disease. In breast cancer patients with bone metastases, denosumab was superior to zoledronic acid in delaying time to first on-study skeletal-related event (SRE; HR=0.82; P=0.01 superiority) and time to first and subsequent on-study SREs (HR=0.77; P=0.001). Overall survival, disease progression, and serious adverse events were similar between groups.
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