Abstract

Multiple myeloma (MM) is amalignancy of hematopoetic system and is associated with destruction of bone, suppressed bone marrow function and renal failure. It is characterized by strong proliferation of malignant plasma cells. Classic therapies contained an alkylating agent and aglucocorticoid. In the 1990s, treatments were supplemented with transplantation of peripheral blood stem cells. During the 2000s, new therapies emerged, combining an immunomodulator (thalidomide, lenalidomide or pomalidomide), aproteasome inhibitor (bortezomib, carfilzomib or ixazomib), and amonoclonal antibody against CD38. Currently, antibodies against BCMA (B-cell maturation antigen), bispecific antibodies, and CAR T‑cell (chimeric antigen receptor T cells) therapies are being investigated in clinical trials. Classic diagnostics were based on end-organ damage, e.g., bone destruction, and estimated tumor load. Since 2014, new criteria for an earlier start of therapy were introduced-concentration of antibody light chains in blood serum, bone marrow lesions and its infiltration by malignant plasma cells. These lesions (clusters of myeloma cells) can be detected by magnetic resonance imaging (MRI) or positron emission tomography/computed tomography (PET/CT). Both methods are also used to monitor therapy response. Traditional X‑ray imaging has been replaced by the more gentle, low-dose CT. The standard diagnostic process is extended by cytogenetic examination of bone marrow samples via imaging fluorescent in situ hybridization (iFiSH) to identify patients at high risk. While most MM patients could be treated only palliatively until the 1990s, the prognosis has continuously improved since then. Nowadays, MM can be classified as achronic disease.

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