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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.

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.

Alessandra Tedeschi, MD
No relevant relationships to disclose.

Marco Montillo, MD
Paid Consultant – Bayer HealthCare AG
Speaker’s Bureau – Bayer HealthCare AG

Barbara Eichhorst, MD
Research Funding – Mundipharma International Limited, Roche Pharmaceuticals
Speaker’s Bureau – Bayer HealthCare AG, Roche Pharmaceuticals

Michael Hallek, MD
Research Funding – Amgen, Bayer HealthCare AG, Mundipharma International Limited, Roche Pharmaceuticals
Speaker’s Bureau – Amgen, Bayer HealthCare AG, Mundipharma International Limited, Roche Pharmaceuticals

Dale L. Bixby, MD, PhD
No relevant relationships to disclose

Sami N. Malek, MD
Research Funding – Affymetrix Inc.
Paid Consultant – Celgene Corporation; Cephalon, Inc.; Research Triangle Institute
Speaker’s Bureau – Celgene Corporation; Cephalon, Inc.

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 newsletter for FDA-approved dosing, indications, and warnings.

Commercial Support
An educational grant for this activity was provided by Bayer HealthCare Pharmaceuticals.

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Illustration

Chronic lymphocytic leukemia (CLL) is a heterogeneous disease with a variable clinical course that is associated with diverse responses to standard therapies, disease progression, and survival. A molecular definition of the spectrum of CLL illnesses is becoming possible by using integrated genomic profiling platforms, with profound implications for prognostication and designing risk-adapted strategies. The clinical diversity of CLL was exemplified by the seminal work of Dr. Döhner and colleagues, who identified genetic lesions that have significant prognostic value in terms of overall survival, with deletion of chromosome 17p (del[17p]) and del(11q) lesions emerging as the predominant negative prognostic factors and normal karyotypes or del(13q14) lesions showing favorable prognosis. Further characterization of del(13q14) genomic lesions identified molecular subtypes that could be classified into type I and type II subgroups with either retinoblastoma gene retention or loss, respectively. This figure shows clustering of heat map displays of copy number estimates for all patients at the 13q14.3 locus in the study, with each column representing a patient, copy losses displayed in blue, and copy gains displayed in red. Based on breakpoint mapping for 13q14 type I deletions using genomic Southern blotting, gene locations and orientations are depicted (far right). In this issue of CLL: The Cutting Edge, Drs. Bixby and Malek review progress in the current understanding of the genomic and molecular basis of CLL.

Ouillette P, et al. Integrated genomic profiling of chronic lymphocytic leukemia identifies subtypes of deletion 13q14. Cancer Res 2008; 68:1012-21.

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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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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.

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Editor, Chronic lymphocytic Leukemia: The Cutting Edge
Physicians’ Education Resource
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Phone: (214) 367–3456
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E–mail: editor@pergrouplp.com

About the Illustration About the Illustration:

Chronic lymphocytic leukemia (CLL) is a heterogeneous disease with a variable clinical course that is associated with diverse responses to standard therapies, disease progression, and survival. A molecular definition of the spectrum of CLL illnesses is becoming possible by using integrated genomic profiling platforms, with profound implications for prognostication and designing risk-adapted strategies. The clinical diversity of CLL was exemplified by the seminal work of Dr. Döhner and colleagues, who identified genetic lesions that have significant prognostic value in terms of overall survival, with deletion of chromosome 17p (del[17p]) and del(11q) lesions emerging as the predominant negative prognostic factors and normal karyotypes or del(13q14) lesions showing favorable prognosis. Further characterization of del(13q14) genomic lesions identified molecular subtypes that could be classified into type I and type II subgroups with either retinoblastoma gene retention or loss, respectively. This figure shows clustering of heat map displays of copy number estimates for all patients at the 13q14.3 locus in the study, with each column representing a patient, copy losses displayed in blue, and copy gains displayed in red. Based on breakpoint mapping for 13q14 type I deletions using genomic Southern blotting, gene locations and orientations are depicted (far right). In this issue of CLL: The Cutting Edge, Drs. Bixby and Malek review progress in the current understanding of the genomic and molecular basis of CLL.

Ouillette P, et al. Integrated genomic profiling of chronic lymphocytic leukemia identifies subtypes of deletion 13q14. Cancer Res 2008; 68:1012-21.

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Educational Grants

An educational grant for this activity was provided by:

1. Bayer HealthCare Pharmaceuticals