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Case Studies in Breast Cancer Vol. 6, No. 8

Release Date: December 11, 2008
Expiration Date: December 11, 2009

Publication Overview

Author

Adam Brufsky, MD, PhD

Overview and Purpose

For patients with breast cancer, bone complications present a frequent clinical challenge. Bone metastases, which are commonly seen in patients with breast cancer, can lead to bone pain and morbidity. Additionally, many therapies used in treating patients with early-stage breast cancer can have a deleterious effect on bone density, leading to increased risk of fracture. The recent increase in aromatase inhibitor (AI) therapy, which can decrease bone mineral density and increase fracture rates, requires that physicians examine therapeutic options for the maintenance and restoration of bone health in patients receiving AI therapy. Several bone-targeted agents are under investigation for the prevention of bone loss, including bisphosphonates and receptor activator of nuclear factor-κB ligand inhibitors. The optimal timing and duration of bisphosphonate and novel bonetargeted agent therapy and the role of these agents in the early-stage setting are areas of debate.

The purpose of this activity is to update physicians on clinical data concerning the safety and efficacy of bone-targeted agents for the prevention of bone loss in patients undergoing adjuvant endocrine therapy for early-stage breast cancer.

Target Audience

This activity is intended for medical oncologists involved in the care of patients with breast cancer. No specific skills or knowledge other than a basic training in oncology is required for successful participation in this activity.

Learning Objectives

Upon completion of this educational activity, you should be able to:

  • Discuss the current recommendations for the prevention and treatment of therapy-induced bone loss in patients with breast cancer
  • Evaluate the efficacy of bisphosphonates and novel bone-targeted agents in the prevention of treatment-induced bone loss in patients with early-stage breast cancer
  • Assess the utility of bisphosphonates for the prevention of metastases in patients with early-stage breast cancer

Instructions for Participation

  1. Read the following information before entering the educational activity.
  2. Complete the Pretest.
  3. Study the educational activity.
  4. Complete the CME test.
  5. Answer the evaluation questions.
  6. After successful completion of the CME test and evaluation, you will receive your certificate of credit online.

CME credit will be granted for only 1 form of participation, either online or via the printed publication.

Read all of the conditions in the Activity Terms box below. You must accept the Activity Terms in order to continue:

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It is the policy of Physicians’ Education Resource to ensure balance, independence, objectivity, and scientific rigor in all of its educational activities. As an organization accredited by the Accreditation Council for Continuing Medical Education (ACCME), Physicians’ Education Resource requires everyone who is in a position to control the content of an educational activity, including spouses/partners, to disclose all relevant financial relationships with any commercial interest. The ACCME defines “relevant financial relationships” as financial relationships in any amount occurring within the past 12 months that create a conflict of interest. Physicians’ Education Resource has implemented a mechanism to identify and resolve all conflicts of interest prior to the activity.

Adam Brufsky, MD, PhD
Speaker’s Bureau – AstraZeneca; Eli Lilly and Company; Genentech, Inc.; Novartis Pharmaceuticals Corporation

PER Editorial Staff
No relevant relationships to disclose

This CME activity might include discussion of investigational and/or unlabeled uses of drugs. If the activity includes discussion of investigational and/or unlabeled uses of a drug, specific information is located on the title page. Please refer to the full prescribing information for each drug discussed in this online newsletter for FDA-approved dosing, indications, and warnings.

Commercial Support
An educational grant for this activity was provided by Novartis Oncology.

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Illustration

Bone maintenance results from a delicate balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption, which are both tightly regulated through the maturation and subsequent activation of osteoblast and osteoclast precursors. A decrease in circulating estrogen levels at menopause leads to a rapid loss of bone mineral density and an increase in fracture risk, implicating estrogen in the regulation of bone formation. Studies suggest that estrogen expression can suppress the T-cell and osteoblast-mediated cytokine production necessary to stimulate osteoclast maturation and activation as well as induce apoptotic cell death in mature osteoclasts. Estrogen deprivation leads to increased osteoclastogenesis and activation and decreased osteoclast apoptosis, thus increasing subsequent bone resorption. In addition, estrogen is thought to stimulate osteoblast survival and function, with estrogen deficiency leading to increased osteoblast apoptosis and reduced bone formation. Research is ongoing to understand these complex interactions and identify specific mechanisms by which estrogen receptor signaling controls bone turnover.

Disclaimer

The views and opinions expressed in this activity are those of the authors and do not necessarily reflect the views of the sponsor, supporter, or publisher. Although great care has been taken in compiling and checking the information given in this activity to ensure accuracy, the authors and Physicians’ Education Resource and its servants or agents shall not be responsible or in any way liable for the continued currency of the information or for any errors, omissions, or inaccuracies in this activity, whether arising from negligence or otherwise howsoever or for any consequences arising therefrom.

Please consult full prescribing information for any drugs or procedures discussed within.

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Editor, Case Studies in Breast Cancer
Physicians’ Education Resource
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