Abstract
Multiple myeloma (MM) is a disease that affects plasma cells and can lead to devastating clinical features such as anemia, lytic bone lesions, hypercalcemia, and renal disease. An enhanced understanding of MM disease mechanisms has led to new more targeted treatments. There is now a plethora of treatments available for MM. In this review article, our aim is to discuss many of the novel agents that are being studied or have recently been approved for the treatment of MM. These agents include the following: immunomodulators (pomalidomide), proteasome inhibitors (carfilzomib, marizomib, ixazomib, oprozomib), alkylating agents (bendamustine), AKT inhibitors (afuresertib), BTK inhibitors (ibrutinib), CDK inhibitors (dinaciclib), histone deacetylase inhibitors (panobinostat, rocilinostat, vorinostat), IL-6 inhibitors (siltuximab), kinesin spindle protein inhibitors (filanesib), monoclonal antibodies (daratumumab, elotuzumab, indatuximab, SAR650984), and phosphoinositide 3-kinase (PI3K) inhibitors.
Highlights
Multiple myeloma (MM) is the second most common hematologic malignancy and accounts for as many as 20 % of deaths from hematological malignancies and 2 % of deaths from all cancers
MM may result from the generation and proliferation of malignant plasma cell clones from germinal center lymphocytes, a process that is driven by multiple factors including interleukin 6 (IL-6) and tumor necrosis factor (TNF) alpha
MM is a consequence of the malignant transformation of post-germinal center plasma cells, via a proposed two-step model of progression [2]
Summary
Multiple myeloma (MM) is the second most common hematologic malignancy and accounts for as many as 20 % of deaths from hematological malignancies and 2 % of deaths from all cancers. In 2012, there were an estimated 89,658 people living with myeloma in the USA. MM may result from the generation and proliferation of malignant plasma cell clones from germinal center lymphocytes, a process that is driven by multiple factors including interleukin 6 (IL-6) and tumor necrosis factor (TNF) alpha. MM is a consequence of the malignant transformation of post-germinal center plasma cells, via a proposed two-step model of progression [2]. An abnormal response to antigenic stimulation foments limited clonal proliferation and precipitates the premalignant entity of monoclonal gammopathy of undetermined
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