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Prepublished online as a Blood First Edition Paper on September 11, 2003; DOI 10.1182/blood-2003-04-1045. This Article Full Text (PDF) All Versions of this Article: 2003-04-1045v1 103/1/20    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Barlogie, B. Articles by Crowley, J. Search for Related Content PubMed PubMed Citation Articles by Barlogie, B. Articles by Crowley, J. Social Bookmarking                   What's this? Submitted April 7, 2003 Accepted July 28, 2003 Treatment of multiple myeloma Bart Barlogie*, John D Shaughnessy, Guido Tricot, Joth Jacobson, Maurizio Zangari, Elias Anaissie, Ron Walker, and John Crowley Myeloma Institute for Research and Therapy, Little Rock, AR, USA Cancer Research and Biostatistics, Seattle, WA, USA * Corresponding author; email: barlogiebart{at}uams.edu. Autologous peripheral blood stem cell (PBSC)-supported high-dose melphalan is now considered standard therapy for myeloma, at least for younger patients. The markedly reduced toxicity of allotransplants utilizing non-myeloablative regimens (mini-allotransplants) may hold promise for more widely exploiting the well-documented graft-versus-myeloma (GVM) effect. New active drugs include immunomodulatory agents, such as thalidomide and Revimid®, and the proteasome inhibitor, PS 341 (Velcade®), all of which not only target myeloma cells directly but also exert an indirect effect by suppressing growth and survival signals elaborated by the bone marrow microenvironment interaction with myeloma cells. Among the prognostic factors evaluated, cytogenetic abnormalities (CA), present in one-third of newly diagnosed patients, identify a particularly poor prognosis subgroup with a median survival not exceeding 2 to 3 years; by contrast, in the absence of CA, 4-year survival rates of 80% - 90% can be obtained with tandem autotransplants. Fundamental and clinical research should therefore focus on the molecular and biological mechanisms of treatment failure in the high risk subgroup. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. K Kettle, K. L Finkbiner, S. 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