Although the incidence of multiple myeloma (MM) is increasing, the median overall survival and the number of agents in the pipeline for treating MM also are increasing. Response rates higher than 80% are not uncommon in the frontline setting when the novel agents thalidomide, lenalidomide, and bortezomib are used in combination. Response rates and survival also have improved in disease that has relapsed after treatment with conventional therapies. The focus of research has now shifted to improving survival and disease response in patients refractory to current treatment paradigms. New agents are targeting new pathways, as well as existing mechanisms known to be effective, but with different safety profiles. Carfilzomib is a potent, selective, irreversible inhibitor of the ubiquitin-proteasome pathway. The drug is a next-generation proteasome inhibitor found to be safe and effective for patients with relapsed and refractory MM, where treatment options are limited. As with any newly approved agent, one should recognize that drugs within the same class will be administered differently and often cause dissimilar treatment-related toxicities. Oncology nurses are crucial to the successful administration of chemotherapeutic agents such as carfilzomib, and an understanding of management techniques is paramount to quality patient care.
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http://dx.doi.org/10.1188/13.CJON.E35-E44 | DOI Listing |
Presse Med
December 2024
Sorbonne Université, Centre de Recherche Saint-Antoine INSERM UMRs938, Service d'Hématologie Clinique et de Thérapie Cellulaire, Hôpital Saint Antoine, AP-HP, Paris, France. Electronic address:
Minimal Residual Disease (MRD) in multiple myeloma has emerged as a significant prognostic factor, guiding treatment strategies and enhancing patient outcomes. Despite advancements in therapies such as proteasome inhibitors, immunomodulatory drugs, monoclonal antibodies, CAR-T cell therapy, and bispecific antibodies, complete eradication of malignant plasma cells remains challenging. MRD refers to a small number of residual cancer cells that persist after treatment and require sensitive methods like next-generation flow cytometry (NGF) and next-generation sequencing (NGS) for detection.
View Article and Find Full Text PDFEur J Med Chem
January 2025
Tarifa Memorial Institute of Pharmacy, Department of Pharmaceutical Chemistry, Murshidabad, 742166, West Bengal, India.
One of the major obstacles to sustained cancer treatment effectiveness is the development of medication resistance. Current therapies that block proteins associated with cancer progression often lose their efficacy due to acquired drug resistance, which is frequently driven by mutated or overexpressed protein targets. Proteolysis-targeting chimeras (PROTACs) offer an alternative therapeutic strategy by hijacking the cell's ubiquitin-proteasome system to degrade disease-causing proteins, presenting several potential advantages.
View Article and Find Full Text PDFClin Exp Med
November 2024
Department of Hematology, Zhongshan Hospital Fudan University, Shanghai, China.
Minimal residual disease (MRD) is of growing interest in light chain (AL) amyloidosis and is associated with higher rates of cardiac response. A new graded cardiac response criteria has been proposed for better assessment of cardiac improvement. We evaluated MRD status in 63 patients with cardiac AL amyloidosis using next generation flow cytometry (sensitivity ≥ 1*10) within four cycles after treatment initiation and cardiac response kinetics.
View Article and Find Full Text PDFLife Sci
December 2024
Department of Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA. Electronic address:
Annu Rev Cancer Biol
June 2024
Department of Medicine, Mayo Clinic, Scottsdale, Arizona, USA.
Recent therapeutic advances have significantly improved the outcome for patients with multiple myeloma (MM). The backbone of successful standard therapy is the combination of Ikaros degraders, glucocorticoids, and proteasome inhibitors that interfere with the integrity of myeloma-specific superenhancers by directly or indirectly targeting enhancer-bound transcription factors and coactivators that control expression of MM dependency genes. T cell engagers and chimeric antigen receptor T cells redirect patients' own T cells onto defined tumor antigens to kill MM cells.
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