Originally published as JCO Early Release 10.1200/JCO.2007.11.6863 on December 3 2007

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Stem-Cell Transplantation for Multiple Myeloma in the Era of Novel Drugs

William Bensinger

From the Fred Hutchinson Cancer Research Center, Seattle, WA

Corresponding author: William Bensinger, MD, D5-390, 1100 Fairview Avenue N, Seattle, WA 98118; e-mail: wbensing{at}fhcrc.org

The treatment of multiple myeloma (MM) is changing rapidly. During the last 10 years, higher rates of complete response (CR) and prolonged progression-free and overall survival have been seen with high-dose chemotherapy plus autologous stem-cell transplantation (HDT-ASCT). Achievement of CR and good partial response have been shown to be key prognostic factors for prolonged survival, with eradication of minimal residual disease seeming crucial to long-term disease-free survival. Until recently, high rates of CR and other major responses were primarily seen with HDT-ASCT, but insights into the biology of MM have led to the development and approval of new drugs with significant activity, and new induction regimens based on these novel agents are offering improved responses. Thalidomide, bortezomib, and lenalidomide have been combined with corticosteroids, alkylators, and anthracyclines in front-line MM treatment. Phase II studies have indicated that high rates of response and CR may be achieved. The substantial activity seen with these new drug combinations has prompted a re-examination of the role of SCT in MM treatment. Will achievement of major responses with these new regimens translate into improved survival after consolidation with transplantation? Will these improved induction regimens reduce the need for tandem transplantation, or does achievement of CR obviate the need for front-line transplantation altogether? To help address these questions, randomized trials are needed, as well as tests with improved sensitivity to better define depth of remission.

published online ahead of print at www.jco.org on December 3, 2007.

Supported in part by Grants No. CA-18029, CA-47748, CA-18221, and CA-15704 from the National Cancer Institute, and HL 36,444 from the National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD; and the Jose Carreras Foundation Against Leukemia, Barcelona, Spain.

Author's disclosures of potential conflicts of interest and author contributions are found at the end of this article.

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