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[Cancer Research 64, 1546-1558, February 15, 2004]
© 2004 American Association for Cancer Research

Meeting Report

Genetics and Cytogenetics of Multiple Myeloma

A Workshop Report

Rafael Fonseca1,11, Bart Barlogie2, Regis Bataille3, Christian Bastard3, P. Leif Bergsagel4, Marta Chesi4, Faith E. Davies5, Johannes Drach6, Philip R. Greipp1, Ilan R. Kirsch7, W. Michael Kuehl7, Jesus M. Hernandez8, Stephane Minvielle3, Linda M. Pilarski9, John D. Shaughnessy, Jr.2, A. Keith Stewart10 and Herve Avet-Loiseau3

1 Division of Hematology, Mayo Clinic, Rochester, Minnesota; 2 University of Arkansas for Medical Science, Little Rock, Arkansas; 3 Institute of Biology, Nantes, France; 4 Cornell Medical Center, New York, New York; 5 University of Leeds and Leeds General Infirmary, Leeds, West Yorkshire, United Kingdom; 6 University of Vienna, Vienna, Austria; 7 National Cancer Institute, NIH, Bethesda, Maryland; 8 Hospital Universitario de Salamanca, Salamanca, Spain; 9 University of Alberta, Edmonton, Alberta, Canada; 10 Princess Margaret Hospital, Toronto, Ontario, Canada; and 11 Division of Hematology and Oncology, Mayo Clinic, Scottsdale, Arizona

ABSTRACT

Much has been learned regarding the biology and clinical implications of genetic abnormalities in multiple myeloma. Because of recent advances in the field, an International Workshop was held in Paris in February of 2003. This summary describes the consensus recommendations arising from that meeting with special emphasis on novel genetic observations. For instance, it is increasingly clear that translocations involving the immunoglobulin heavy-chain locus are important for the pathogenesis of one-half of patients. As a corollary, it also clear that the remaining patients, lacking IgH translocations, have hyperdiploidy as the hallmark of their disease. Several important genetic markers are associated with a shortened survival such as chromosome 13 monosomy, hypodiploidy, and others. The events leading the transformation of the monoclonal gammopathy of undetermined significance (MGUS) to myeloma are still unclear. One of the few differential genetic lesions between myeloma and MGUS is the presence of ras mutations in the latter. Gene expression platforms are capable of detecting many of the genetic aberrations found in the clonal cells of myeloma. Areas in need of further study were identified. The study of the genetic aberrations will likely form the platform for targeted therapy for the disease.




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N. C. Gutierrez, J. L. Garcia, J. M. Hernandez, E. Lumbreras, M. Castellanos, A. Rasillo, G. Mateo, J. M. Hernandez, S. Perez, A. Orfao, et al.
Prognostic and biologic significance of chromosomal imbalances assessed by comparative genomic hybridization in multiple myeloma
Blood, November 1, 2004; 104(9): 2661 - 2666.
[Abstract] [Full Text] [PDF]

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C. A. Maxwell, E. Rasmussen, F. Zhan, J. J. Keats, S. Adamia, E. Strachan, M. Crainie, R. Walker, A. R. Belch, L. M. Pilarski, et al.
RHAMM expression and isoform balance predict aggressive disease and poor survival in multiple myeloma
Blood, August 15, 2004; 104(4): 1151 - 1158.
[Abstract] [Full Text] [PDF]

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J.-L. Harousseau, J. Shaughnessy Jr., and P. Richardson
Multiple Myeloma
Hematology, January 1, 2004; 2004(1): 237 - 256.
[Abstract] [Full Text] [PDF]


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