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Cancer Summaries & Commentaries Vol. 1, No. 5

Summaries of Selected Presentations From the 33rd ESMO Congress
Stockholm, Sweden; September 12-16, 2008
This activity is not sanctioned by, nor a part of, the 33rd ESMO Congress.

Release Date: December 17, 2008
Expiration Date: December 17, 2009

Publication Overview

Authors

Medical writer: Paul Card, PhD; Medical writer: Tristin Abair, PhD; Reviewed by: Debu Tripathy, MD

Overview and Purpose

The treatment of metastatic breast cancer (MBC) has evolved rapidly over the past decade, with a variety of combinations of targeted agents and newer cytotoxic drugs being continually evaluated in the first-line setting or following disease progression. Chemotherapy is still the mainstay of treatment, and the development of regimens and combinations to optimize the therapeutic ratio of efficacy to toxicity is an active area of research. Biologic agents, such as antibodies and small-molecule tyrosine kinase inhibitors (TKIs) of HER2, vascular endothelial growth factor (VEGF), and VEGF receptor, are becoming an increasingly important part of the management of MBC. However, it is important to also evaluate issues such as quality of life (QOL) as these new agents are added to the treatment armamentarium. De novo or acquired resistance has prompted research into various combinations using targeted agents and/or cytotoxic drugs to improve tumor response and to prevent or overcome the development of resistance. Strategies using targeted agents alone to increase blockade of a single pathway or to simultaneously inhibit signaling from multiple pathways are also being investigated. Finally, algorithms to accurately predict the potential for organ-specific metastatic lesions are also being developed, with the long-term goal of identifying prophylactic strategies for patients at high risk. The rapidly changing landscape of care for MBC makes it imperative that clinicians continually update themselves on the latest developments in therapy and management of patients with MBC.

The purpose of this activity is to apprise physicians of current data on the use of new combination therapies, QOL monitoring, and new predictive tools to improve the management of advanced 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:

  • Assess the potential impact on QOL of adding an antiangiogenic agent to a taxane in the treatment of locally recurrent/metastatic breast cancer
  • Compare the efficacy and safety of first-line taxane/anthracycline therapy to that of taxane/antimetabolite therapy in patients with locally advanced/metastatic breast cancer
  • Evaluate the efficacy and safety of combining 2 anti-HER2 antibodies in the treatment of HER2+ MBC that has progressed on prior regimens using a single-antibody HER2 inhibitor
  • Evaluate the activity and safety of dual HER1/HER2 and VEGF inhibition using small-molecule TKIs as first-line therapy for HER2+ locally advanced/metastatic breast cancer
  • Appraise the preliminary efficacy and safety of combining an anti-HER1/HER2 small-molecule TKI with an antiangiogenic antibody in the treatment of HER2+ MBC
  • Evaluate the ability of a nomogram to predict the risk of brain metastases in patients with MBC

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:

Disclosure Policy

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.

Howard A. Burris III, MD, FACP
Paid Consultant – Bristol-Myers Squibb Company; Genentech, Inc.; GlaxoSmithKline; Novartis Pharmaceuticals Corporation; sanofi - aventis U.S.

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 Genentech BioOncology.

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Illustration

Angiogenesis is required for tumor growth and progression and is now a target for antitumor therapies. The development of blood vessels is a complex process involving activation and downregulation of multiple signaling molecules, including receptor tyrosine kinases such as vascular endothelial growth factor receptors (VEGFRs). VEGFR-2 can homodimerize or heterodimerize with VEGFR-1 upon ligand stimulation, leading to phosphorylation of tyrosine residues and activation of the kinase domain of VEGFR-2. This results in activation of multiple downstream signaling pathways involved in cellular processes, such as endothelial cell survival, proliferation, and migration, which are all necessary for vascularization. Negative feedback to VEGFR signaling is provided through ligand-dependent downregulation of VEGFR-2, which is thought to occur through activation of PKC by VEGFR-2. Two serine residues in the carboxyl terminus of the cytoplasmic domain of VEGFR-2 are subsequently phosphorylated by either PKC or a downstream effector of PKC. These phosphorylated serine residues can then recruit an E3 ligase, leading to ubiquitination of VEGFR-2 and subsequent degradation by the proteasome. Further studies are needed to determine the precise signaling molecules involved in this negative feedback loop and how they interact to control aberrant blood vessel development.

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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©Copyright 2008 by Physicians’ Education Resource. No material may be reproduced in whole or in part, in any form, without written permission from the publisher.

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Editor, Cancer Summaries & Commentaries
Physicians’ Education Resource
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Suite 700
Dallas, TX 75219
Phone: (214) 367–3400
Fax: (214) 367–3304
E–mail: editor@cancerlearning.com

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Educational Grants

An educational grant for this activity was provided by:


  1. Genentech BioOncology