Extramedullary disease in multiple myeloma: a systematic literature review.

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Abstract

[Indexed for MEDLINE] Conflict of interest statement: J.B. has received speaker/lecture honoraria from Janssen, Celgene/BMS, Amgen, Takeda, and Oncopeptides. M.B. has received speaker honoraria from Amgen, Oncopeptides, Janssen, Sanofi, and Takeda. Jo Caers has received research funding from Takeda and Janssen; and honoraria from Janssen, Amgen, BMS-Celgene, and Sanofi. A.J. has received honoraria from Janssen, BMS, Takeda, Sanofi, GSK, Karyopharm, Oncopeptides, and Amgen. M.v.L.-T. has received research funding from Celgene and Oncopeptides; and honoraria from BMS/Celgene, Oncopeptides, Janssen, GSK, and Takeda. Philippe Moreau has received honoraria from Janssen, Celgene, Amgen, AbbVie, Oncopeptides, and Sanofi. Leo Rasche has received honoraria from BMS/Celgene, Sanofi, GSK, Oncopeptides, and Janssen. Laura Rosiñol has received speaker honoraria from Janssen, Celgene, Amgen, Takeda, GSK, and Sanofi. S.Z.U. has received research funding and/or honoraria from Amgen, Celgene, Janssen, Takeda, BMS, Oncopeptides, and Sanofi. E.Z. has received honoraria from, and been an advisory board member for, Janssen, BMS, Takeda, Sanofi, GSK, Karyopharm, Oncopeptides, and Amgen. P.R. has received institutional research support from Oncopeptides, Celgene/BMS, Takeda, and Karyopharm. He has received honoraria for his role as an Advisory Committee member from Karyopharm, Oncopeptides, Celgene/BMS, Takeda, Janssen, Sanofi, Secura Bio, GSK, Regeneron, AstraZeneca, and Protocol Intelligence. 3. Clin J Am Soc Nephrol. 2006 Nov;1(6):1322-30. doi: 10.2215/CJN.03060906. Epub 2006 Oct 11. Multiple myeloma. Singhal S(1), Mehta J. Author information: (1)Division of Hematology/Oncology, Department of Medicine, Feinberg School of Medicine, Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois, USA. s-singhal@northwestern.edu Multiple myeloma is a malignant disease characterized by plasmacytosis, paraprotein production, bone lesions, hypercalcemia, susceptibility to infections, and renal impairment. The underlying pathophysiologic phenomena of the clinical features include suppression of humoral- and cell-mediated immunity, elevation of IL-6, abnormalities of the bone marrow microenvironment, and increased osteoclastic activity. Overwhelming predictors of prognosis include albumin, beta2-microglobulin, and chromosomal karyotype. With modern, intensive therapy including autologous hematopoietic stem cell transplantation, the median survival is approximately 5 yr. The disease is incurable and eventually relapses; requiring salvage therapy. The development of newer agents such as thalidomide, bortezomib, and lenalidomide--drugs that interfere with several of the complex pathophysiologic steps--has improved the outlook of relapsed disease significantly. Current studies are directed at exploring the use of these novel agents earlier in the course of therapy, development of newer targeted therapies, and the use of gene expression profiling to individualize therapy. DOI: 10.2215/CJN.03060906