New Developments in Endocrine Therapy and Bone-Targeted Agents for Breast Cancer
Cancer Summaries & Commentaries Vol. 2, No. 1
This activity is not sanctioned by, nor a part of, the 31st Annual San Antonio Breast Cancer Symposium.
Release Date: April 1, 2009
Expiration Date: April 1, 2010
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Kimberly Blackwell, MD
Research Funding – Abraxis Bioscience, LLC; Bristol-Myers Squibb Company; Genentech, Inc.; GlaxoSmithKline
Paid Consultant – Novartis Pharmaceuticals Corporation
Speaker’s Bureau – Novartis Pharmaceuticals Corporation, sanofi-aventis U.S.
PER Editorial Staff
No relevant relationships to disclose
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An educational grant for this activity was provided by Novartis Oncology.
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Illustration
For hormone receptor–positive breast cancer, complex interactions between signaling pathways greatly affect tumor progression and bone health. Bone maintenance results from a delicate balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption, which are both tightly regulated through maturation and subsequent activation of osteoblast and osteoclast precursors. A decrease in circulating estrogen levels due to menopause or endocrine therapy leads to a rapid loss of bone mineral density and an increase in fracture risk, implicating estrogen in the regulation of bone formation. The estrogen signaling pathway is also thought to have substantial cross-talk with the HER2 receptor pathway. Preclinical data demonstrate that upregulation of HER2 might contribute to resistance to endocrine therapy in hormone receptor–positive breast cancer cells, suggesting that coadministration of endocrine therapy with HER2-targeted therapy might circumvent this resistance mechanism. Ongoing studies are examining this dual-inhibition strategy as well as strategies to prevent bone loss in patients with breast cancer.
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