Abstract
Multiple myeloma (MM) is a devastating malignancy of B cells characterized by the proliferation and accumulation of abnormal plasma cells in the bone marrow compartment (1) arising from an asymptomatic premalignant monoclonal plasma cells that are derived from post-germinal center B cells. Multistep genetic and microenvironmental changes lead to the transformation of these cells into a malignant neoplasm (2). It accounts for about 1% of neoplastic maladies and 10% of all hematologic neoplasms. Treatment for MM is focused on therapies that decrease the clonal plasma cell population and consequently decrease the signs and symptoms of disease. The melphalan-prednisolone combination therapy, immunomodulatory drugs like thalidomide and lenalidomide along with proteasome inhibitors (bortezomib) are being employed currently for the treatment of MM (3). These immunomodulatory drugs induce their effect by activation of natural killer (NK) cells, stimulation of CD4+ and CD8+ T cells and inhibition of regulatory T (T-reg) cells (4).
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