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Originally published as JCO Early Release 10.1200/JCO.2008.16.3832 on August 25 2008 © 2008 American Society of Clinical Oncology. Randomized Trial of Denosumab in Patients Receiving Adjuvant Aromatase Inhibitors for Nonmetastatic Breast Cancer
From the Seattle Cancer Care Alliance, Seattle, WA; Michigan Bone and Mineral Clinic, Detroit, MI; University of California at Los Angeles Medical Center, Torrance; Amgen Inc, Thousand Oaks, CA; US Oncology, Houston, TX; Rocky Mountain Cancer Centers, Denver, CO; and Algoma Regional Cancer Program, Sault Ste Marie, Ontario, Canada Corresponding author: Georgiana K. Ellis, MD, Seattle Cancer Care Alliance, 825 Eastlake Ave East, Mail Stop G3-200, Seattle, WA 98109-1023; e-mail: gellis{at}u.washington.edu
Purpose Adjuvant aromatase inhibitor therapy is well established in postmenopausal women with hormone receptor–positive breast cancer, but such therapy is complicated by accelerated bone loss and increased fracture risk. We investigated the ability of denosumab, a fully human monoclonal antibody against receptor activator of nuclear factor-
Patients and Methods Eligible women with hormone receptor–positive nonmetastatic breast cancer treated with adjuvant aromatase inhibitor therapy were stratified by duration of aromatase inhibitor therapy ( Results At 12 and 24 months, lumbar spine BMD increased by 5.5% and 7.6%, respectively, in the denosumab group versus placebo (P < .0001 at both time points). Increases were observed as early as 1 month and were not influenced by duration of aromatase inhibitor therapy. Increases in BMD were also observed at the total hip, total body, femoral neck, and the predominantly cortical one-third radius. Bone turnover markers decreased with denosumab treatment. Overall incidence of treatment-emergent adverse events (AEs) was similar between treatment groups. Conclusion In women with nonmetastatic breast cancer and low bone mass who were receiving adjuvant aromatase inhibitor therapy, twice-yearly administration of denosumab led to significant increases in BMD over 24 months at trabecular and cortical bone, with overall AE rates similar to those of placebo. published online ahead of print at www.jco.org on August 25, 2008 Supported by Amgen Inc, Thousand Oaks, CA. This study is registered with ClinicalTrials.gov with the identifier NCT00089661 [ClinicalTrials.gov] . Presented in part at the San Antonio Breast Cancer Symposium, December 13-16, 2007, San Antonio, TX. Authors’ disclosures of potential conflicts of interest and author contributions are found at the end of this article. Clinical trial information can be found for the following: NCT00089661 [ClinicalTrials.gov] .
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Copyright © 2008 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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B ligand, to protect against aromatase inhibitor–induced bone loss. 
6 v > 6 months), received supplemental calcium and vitamin D, and were randomly assigned to receive placebo (n = 125) or subcutaneous denosumab 60 mg (n = 127) every 6 months. At enrollment, all patients were required to have evidence of low bone mass, excluding osteoporosis. The primary end point was percentage change from baseline at month 12 in lumbar spine bone mineral density (BMD). 
