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Table 1.  

Abnormality Frequency Prognosis
Hyperdiploidy 50%–60% Good/neutral
t(4;14) 15% Poor (neutral if
bortezomib-based
therapy)
t(11;14) 20% Neutral
t(14;16) 3% Poor/neutral
Monosomy 13 45% Neutral
del(17p) 8% Poor
1q gain 35% Poor
del(1p) 30% Poor
5q gain 50% Good
del(12p) 10% Poor

Recurrent Cytogenetic Changes in Myeloma

CME

The Impact of Genomics on the Management of Myeloma

  • Authors: Jill Corre, MD; Hervé Avet-Loiseau, MD, PhD
  • CME Released: 10/7/2011
  • THIS ACTIVITY HAS EXPIRED FOR CREDIT
  • Valid for credit through: 10/7/2012, 11:59 PM EST
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Target Audience and Goal Statement

This activity is intended for oncologists, geneticists, and other physicians who care for patients with multiple myeloma.

The goal of this activity is to evaluate the genomics of multiple myeloma and their clinical applicability.

Upon completion of this activity, participants will be able to:

  1. Distinguish the most common genetic abnormality in multiple myeloma
  2. Analyze how specific genetic abnormalities affect the prognosis of multiple myeloma
  3. Evaluate how genetic findings in multiple myeloma can affect the choice of treatment


Disclosures

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Medscape, LLC, encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content.


Author(s)

  • Jill Corre, MD

    Centre Hospitalier Universitaire, Université, Toulouse, France

    Disclosures

    Disclosure: Jill Corre, MD, has disclosed no relevant financial relationships.

  • Hervé Avet-Loiseau, MD, PhD

    Centre Hospitalier Universitaire, Université, Nantes, France

    Disclosures

    Disclosure: Hervé Avet-Loiseau, MD, PhD, has disclosed no relevant financial relationships.

Editor(s)

  • Kerrin M. Green, MA

    Assistant Managing Editor, Journal of the National Comprehensive Cancer Network

    Disclosures

    Disclosure: Kerrin M. Green, MA, has disclosed no relevant financial relationships.

CME Author(s)

  • Charles P. Vega, MD

    Health Sciences Clinical Professor; Residency Director, Department of Family Medicine, University of California, Irvine

    Disclosures

    Disclosure: Charles P. Vega, MD, has disclosed no relevant financial relationships.

CME Reviewer(s)

  • Nafeez Zawahir, MD

    CME Clinical Director, Medscape, LLC

    Disclosures

    Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.

  • Sarah Fleischman

    CME Program Manager, Medscape, LLC

    Disclosures

    Disclosure: Sarah Fleischman has disclosed no relevant financial relationships.


Accreditation Statements

    For Physicians

  • This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of Medscape, LLC and JNCCN - The Journal of the National Comprehensive Cancer Network. Medscape, LLC is accredited by the ACCME to provide continuing medical education for physicians.

    Medscape, LLC designates this Journal-based CME activity for a maximum of 1.00 AMA PRA Category 1 Credit(s)™ . Physicians should claim only the credit commensurate with the extent of their participation in the activity.

    Medscape, LLC staff have disclosed that they have no relevant financial relationships.

    Contact This Provider

For questions regarding the content of this activity, contact the accredited provider for this CME/CE activity noted above. For technical assistance, contact [email protected]


Instructions for Participation and Credit

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This activity is designed to be completed within the time designated on the title page; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity online during the valid credit period that is noted on the title page. To receive AMA PRA Category 1 Credit™, you must receive a minimum score of 70% on the post-test.

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CME

The Impact of Genomics on the Management of Myeloma

Authors: Jill Corre, MD; Hervé Avet-Loiseau, MD, PhDFaculty and Disclosures
THIS ACTIVITY HAS EXPIRED FOR CREDIT

CME Released: 10/7/2011

Valid for credit through: 10/7/2012, 11:59 PM EST

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Abstract and Introduction

Abstract

Myeloma is a complex disease, characterized by a wide heterogeneity in clinical presentation, evolution, and molecular portraits. The successive use of cytogenetics, molecular cytogenetics, expression genomics, copy number genomics, and, more recently, deep sequencing, has shown that this heterogeneity can be used to identify markers usable for not only prognostication but also therapeutic choice and, ultimately, discovery of druggable targets. The use of some of these techniques is now mandatory for the management of patients. Although risk-adapted therapy is not yet a routine practice in myeloma, these molecular changes are essential for the definition of the prognosis. (JNCCN 2011;9:1200–1207)

Introduction

Despite major improvements in the prognosis of multiple myeloma in the past decade (mainly because of the availability of novel drugs, such as thalidomide, bortezomib, and lenalidomide), patient outcomes are highly heterogeneous. Even though the median survival of the youngest patients is probably now more than 10 years, some patients are still presenting with refractory disease, with a fatal evolution within weeks or months. Many factors can drive this evolution. Apart from patient-related factors, such as comorbidities (including poor performance status and cardiac, renal, or liver dysfunctions), the most important heterogeneity is related to intrinsic malignant plasma cell variations. The basis of this heterogeneity is probably within the wide spectrum of molecular rearrangements observed in the malignant plasma cells. During the past decade, many studies exploring genetic rearrangements have been published. This article addresses the abnormalities that could be used in the management of patients with myeloma.