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Continuing Education Information

Physicians' Education Resource is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Physicians' Education Resource designates this educational activity for a maximum of 1 AMA PRA Category 1 Credit(s)™. Physicians should only claim credit commensurate with the extent of their participation in the activity.

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.

PER Editorial Staff
No relevant relationships to disclose

Satellite Faculty

Joyce O’Shaughnessy, MD
Paid Consultant – Abraxis Oncology; AstraZeneca; Eisai Inc.; Eli Lilly and Company; Genentech, Inc.; Molecular Profiling Institute; Novartis Pharmaceuticals Corporation; Pfizer Inc.; and sanofi-aventis U.S.
Speaker’s Bureau – Abraxis Oncology; AstraZeneca; Eisai Inc.; Eli Lilly and Company; Genentech, Inc.; Molecular Profiling Institute; Novartis Pharmaceuticals Corporation; Pfizer Inc.; sanofi-aventis U.S.

Beth Overmoyer, MD, FACP
Paid Consultant – sanofi-aventis U.S.

Hope S. Rugo, MD
Research Funding – Bristol-Myers Squibb Company; Genentech, Inc.; GlaxoSmithKline; Novartis Pharmaceuticals Corporation; Pfizer Inc.
Speaker’s Bureau – AstraZeneca; Genomic Health, Inc.

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 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

The HER2 receptor tyrosine kinase is important for the development and maintenance of epithelial tissues, and overexpression of this receptor occurs in approximately 20%-25% of breast cancers and is associated with tumor growth, progression, and reduced survival. Following the translation of HER2 mRNA into nascent polypeptide in the endoplasmic reticulum and processing in the Golgi apparatus, the HER2 protein associates with heat shock protein (HSP)90 via a HSP90 recognition motif located within the HER2 kinase domain. This interaction is required for the function of HER2 and stabilizes the receptor prior to insertion into the cell membrane. HER2 has been implicated as one of the most important clients of HSP90, and inhibitors of this chaperone cause the degradation of HER2 and other client proteins involved in tumor-associated signal transduction. Substantial progress has been made over the last decade to inhibit tumor growth using small-molecule– and antibody-based therapies targeting HER2-mediated signaling, and additional efforts are under way to develop therapies targeting related interacting pathways and molecules, such as HSP90, which might further augment the efficacy of current HER2-directed agents.

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.

Privacy Policy

Physicians’ Education Resource (PER) makes reasonable efforts to ensure that privacy issues are handled responsibly. PER does not sell or share your information with other organizations that are not directly involved in this process. If you have further concerns, you may contact us at (888) 949–0045.

All rights reserved. No part of this activity may be translated, reproduced, stored, or transmitted by any means or in any type of media form including electronic, mechanical photocopying, recording, broadcasting, or otherwise without prior permission from the publisher.

©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.

All correspondence should be directed to:
Editor, Expanding Options for the Treatment of Metastatic Breast Cancer
Physicians’ Education Resource
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Suite 700
Dallas, TX 75219
Phone: (214) 367–3456
Fax: (214) 367–3304
E–mail: editor@pergrouplp.com

About the Illustration About the Illustration:

The HER2 receptor tyrosine kinase is important for the development and maintenance of epithelial tissues, and overexpression of this receptor occurs in approximately 20%-25% of breast cancers and is associated with tumor growth, progression, and reduced survival. Following the translation of HER2 mRNA into nascent polypeptide in the endoplasmic reticulum and processing in the Golgi apparatus, the HER2 protein associates with heat shock protein (HSP)90 via a HSP90 recognition motif located within the HER2 kinase domain. This interaction is required for the function of HER2 and stabilizes the receptor prior to insertion into the cell membrane. HER2 has been implicated as one of the most important clients of HSP90, and inhibitors of this chaperone cause the degradation of HER2 and other client proteins involved in tumor-associated signal transduction. Substantial progress has been made over the last decade to inhibit tumor growth using small-molecule– and antibody-based therapies targeting HER2-mediated signaling, and additional efforts are under way to develop therapies targeting related interacting pathways and molecules, such as HSP90, which might further augment the efficacy of current HER2-directed agents.

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Educational Grants

An educational grant for this activity was provided by:

1. Genentech BioOncology