Although survival of multiple myeloma patients has at least doubled during recent years, most patients eventually relapse, and treatment at this stage may be particularly complex. At the time of relapse, the use of alternative drugs to those given upfront is current practice. However, many new options are currently available for the treatment of relapsed multiple myeloma, including recently approved drugs, such as the second- and third-generation proteasome inhibitors carfilzomib and ixazomib, the immunomodulatory agent pomalidomide, the monoclonal antibodies daratumumab and elotuzumab and the histone deacetylase inhibitor panobinostat, but also new targeted agents are under active investigation (e.g. signal transduction modulators, kinesin spindle protein inhibitors, and inhibitors of NF-kB, MAPK, AKT). We here describe a new paradigm for the treatment of relapsed multiple myeloma. The final goal should be finding a balance among efficacy, toxicity, and cost and, at the end of the road, achieving long-lasting control of the disease and eventually even cure in a subset of patients.
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http://dx.doi.org/10.1007/s40265-017-0841-y | DOI Listing |
J Comput Biol
December 2024
Biotechnology Institute, Universidad Nacional de Colombia, Bogota, Colombia.
In this study, we develop a comprehensive model to investigate the intricate relationship between the bone remodeling process, tumor growth, and bone diseases such as multiple myeloma. By analyzing different scenarios within the Basic Multicellular Unit, we uncover the dynamic interplay between remodeling and tumor progression. The model developed developed in the paper are based on the well accepted Komarova's and Ayati's models for the bone remodeling process, then these models were modified to include the effects of the tumor growth.
View Article and Find Full Text PDFOncoimmunology
December 2025
Cancer Immunotherapy Unit (UNICA), Department of Immunology, Hospital Universitario12 de Octubre, Madrid, Spain.
Despite recent advances in immunotherapy against B cell malignancies such as BCMA (B cell maturation antigen) and CD19-targeted treatments using soluble T cell-engaging (TCE) antibodies or chimeric antigen receptor T cells (CAR-T), there is still an important number of patients experiencing refractory/relapsed (R/R) disease. Approaches to avoid tumor-intrinsic mechanisms of resistance such as immune pressure-mediated antigen downmodulation, are being broadly investigated. These strategies include BCMA/CD19 dual-targeting therapies, which may be of particular interest to patients with B cell lymphoma and multiple myeloma, where a specific double-positive immature subpopulation is commonly associated with poor prognosis and poor response to current treatments.
View Article and Find Full Text PDFFront Oncol
December 2024
Atrium Health Levine Cancer Institute, Wake Forest University School of Medicine, Charlotte, NC, United States.
Pharmgenomics Pers Med
December 2024
Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: Multiple myeloma (MM) is a hematological malignancy characterized by the clonal proliferation of malignant plasma cells within the bone marrow. The disease's complexity is underpinned by a variety of genetic and molecular abnormalities that drive its progression.
Methods: This review was conducted through a state-of-The-art literature search, primarily utilizing PubMed to gather peer-reviewed articles.
Semin Hematol
November 2024
Division of Hematology and Medical Oncology, Icahn School of Medicine at Mount Sinai, New York, NY. Electronic address:
Etiological links to multiple myeloma (MM) remain poorly understood, though emerging evidence suggests a significant hereditary component. This review integrates current literature on inherited factors contributing to MM risk, synthesizing both epidemiologic and genomic data. We examine familial clustering patterns, assess genome-wide association studies (GWAS) that reveal common genetic variants linked to MM, and explore rare, high-penetrance variants in key susceptibility genes.
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