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Am Soc Clin Oncol Educ Book ; 37: 561-568, 2017.
Artículo en Inglés | MEDLINE | ID: mdl-28561703

RESUMEN

Multiple myeloma (MM) is a plasma cell malignancy characterized by the growth of tumor cells in the bone marrow. Properties of the tumor microenvironment provide both potential tumor-promoting and tumor-restricting properties. Targeting underlying immune triggers for evolution of tumors as well as direct attack of malignant plasma cells is an emerging focus of therapy for MM. The monoclonal antibodies daratumumab and elotuzumab, which target the plasma cell surface proteins CD38 and SLAMF7/CS1, respectively, particularly when used in combination with immunomodulatory agents and proteasome inhibitors, have resulted in high response rates and improved survival for patients with relapsed and refractory MM. A number of other monoclonal antibodies are in various stages of clinical development, including those targeting MM cell surface antigens, the bone marrow microenvironment, and immune effector T cells such as antiprogrammed cell death protein 1 antibodies. Bispecific preparations seek to simultaneously target MM cells and activate endogenous T cells to enhance efficacy. Cellular immunotherapy seeks to overcome the limitations of the endogenous antimyeloma immune response through adoptive transfer of immune effector cells with MM specificity. Allogeneic donor lymphocyte infusion can be effective but can cause graft-versus-host disease. The most promising approach appears to be genetically modified cellular therapy, in which T cells are given novel antigen specificity through expression of transgenic T-cell receptors (TCRs) or chimeric antigen receptors (CARs). CAR T cells against several different targets are under investigation in MM. Infusion of CD19-targeted CAR T cells following salvage autologous stem cell transplantation (SCT) was safe and extended remission duration in a subset of patients with relapsed/refractory MM. CAR T cells targeting B-cell maturation antigen (BCMA) appear most promising, with dramatic remissions seen in patients with highly refractory disease in three ongoing trials. Responses are associated with degree of CAR T-cell expansion/persistence and often toxicity, including cytokine release syndrome (CRS) and neurotoxicity. Ongoing and future studies are exploring correlates of response, ways to mitigate toxicity, and "universal" CAR T cells.


Asunto(s)
Neoplasias Hematológicas/genética , Neoplasias Hematológicas/terapia , Inmunoterapia , Trasplante de Células Madre , ADP-Ribosil Ciclasa 1/antagonistas & inhibidores , ADP-Ribosil Ciclasa 1/genética , Anticuerpos Monoclonales/uso terapéutico , Terapia Combinada , Neoplasias Hematológicas/inmunología , Neoplasias Hematológicas/patología , Humanos , Glicoproteínas de Membrana/antagonistas & inhibidores , Glicoproteínas de Membrana/genética , Células Plasmáticas/efectos de los fármacos , Células Plasmáticas/patología , Receptores de Antígenos de Linfocitos T/antagonistas & inhibidores , Familia de Moléculas Señalizadoras de la Activación Linfocitaria/antagonistas & inhibidores , Familia de Moléculas Señalizadoras de la Activación Linfocitaria/genética , Linfocitos T/inmunología , Microambiente Tumoral/efectos de los fármacos
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