Abstract
Multiple myeloma (MM) is a B-cell neoplasm in which malignant plasma cells accumulate in the bone marrow and produce lytic bone lesions and excessive amounts of a monoclonal protein (usually an immunoglobulin of the IgG or IgA type or free light chain). Approximately 14,000 new cases of MM are diagnosed each year in the United States, and the disease accounts for approx 1.9% of all cancer-related deaths (1,2). Despite significant advances in therapy, the disease remains essentially incurable. The therapy of choice in younger patients is currently high-dose therapy with autologous stem cell transplantation; however, a range of novel therapeutic options have recently become available, creating new opportunities for clinical investigation. The major challenge facing clinicians is to determine which of these new agents or which combination of agents will prove to be the most effective and result in a cure for even a small proportion of patients.
References
Greenlee R. T., Hill-Harmon M. B., Murray T., and Thun M. (2001) Cancer statistics, 2001. CA Cancer J. Clin. 2001 51, 15ā36.
Ries L. A. G., Eisner M. P., and Kosary C. L. (2002) SEER Cancer Statistics Review, 1973ā1999. National Cancer Institute, Bethesda, MD.
BarillĆ©-Nion S., Barlogie B., Bataille R., et al. (2003) Advances in biology and therapy of multiple myeloma. Hematology (Am. Soc. Hematol. Educ. Program) 2003, 248ā278.
Richardson P., Schlossman R., Weller E., et al. (2002) Immunomodulatory drug CC-5013 overcomes drug resistance and is well tolerated in patients with relapsed multiple myeloma. Blood 100, 3063ā3067.
Richardson P. G., Barlogie B., Berenson J., et al. (2003) A phase 2 study of bortezomib in relapsed, refractory myeloma. N. Engl. J. Med. 348, 2609ā2617.
Santucci R., Mackley P. A., Sebti S., and Alsina M. (2003) Farnesyltransferase inhibitors and their role in the treatment of multiple myeloma. Cancer Control 10, 384ā387.
Liu Q. and Gazitt Y. (2003) Potentiation of dexamethasone-, paclitaxel-, and Ad-p53-induced apoptosis by Bcl-2 antisense oligodeoxynucleotides in drugresistant multiple myeloma cells. Blood 101, 4105ā4114.
Trudel S., Ely S., Farooqi Y., Affer M., Robbiani D. F., and Bergsagel P. (2004) Inhibition of fibroblast growth factor receptor 3 induces differentiation and apoptosis in t(4;14) myeloma. Blood 103, 3521ā3528.
Podar K., Catley L. P., Tai Y. T., et al. (2004) The pan-inhibitor of VEGF receptors GW654652 blocks growth and migration of multiple myeloma cells in the bone marrow microenvironment. Blood 103, 3474ā3479.
Facon T., Avet-Loiseau H., Guillerm G., et al. (2001) Chromosome 13 abnormalities identified by FISH analysis and serum beta2-microglobulin produce a powerful myeloma staging system for patients receiving high-dose therapy. Blood 97, 1566ā1571.
Desikan R., Barlogie B., Sawyer J., et al. (2000) Results of high-dose therapy for 1000 patients with multiple myeloma: durable complete remissions and superior survival in the absence of chromosome 13 abnormalities. Blood 95, 4008ā4010.
Zhan F., Tian E., Bumm K., Smith R., Barlogie B., and Shaughnessy J., Jr. (2003) Gene expression profiling of human plasma cell differentiation and classification of multiple myeloma based on similarities to distinct stages of late-stage B-cell development. Blood 101, 1128ā1140.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
Ā© 2005 Humana Press Inc.
About this protocol
Cite this protocol
Joshua, D., Brown, R., Ho, P.J. (2005). Multiple Myeloma. In: Brown, R.D., Ho, P.J. (eds) Multiple Myeloma. Methods in Molecular Medicineā¢, vol 113. Humana Press. https://doi.org/10.1385/1-59259-916-8:1
Download citation
DOI: https://doi.org/10.1385/1-59259-916-8:1
Publisher Name: Humana Press
Print ISBN: 978-1-58829-392-3
Online ISBN: 978-1-59259-916-5
eBook Packages: Springer Protocols