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Bortezomib is an efficient agent in plasma cell leukemias
Open accessAbstract
Plasma cell leukemia (PCL) represents the most aggressive form of monoclonal gammopathy for which new treatment approaches are needed. Here we report the effect of Bortezomib on cells from 4 patients with PCL, as well as the in vivo efficacy on a patient with secondary PCL. Bortezomib reduced PCL numbers and was more efficient in cell growth inhibition than dexamethasone or doxorubicin. Treatment with Bortezomib induced procaspase‐3 and poly(ADP‐ribose) polymerase cleavage and decreased the amount of extracellular signal regulated kinase (Erk1/2) and phospho‐Erk1/2. However, Bortezomib did not substantially affect the levels of the Erk1/2 upstream activating kinase (MEK1), p27 or p21. Finally, we had the opportunity to use Bortezomib in a heavily pretreated patient with overt secondary PCL and severe anemia and thrombocytopenia. Following Bortezomib treatment, circulating plasma cells disappeared; what is more striking, the peripheral blood counts returned to normal, becoming transfusion‐independent. These data support the inclusion of Bortezomib in the therapeutic armamentarium of PCL. © 2005 Wiley‐Liss, Inc.
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Previous studies across multiple tumor types have reported variable effects of bortezomib on MAPK signaling.
“Previous studies across multiple tumor types including breast cancer, plasma cell leukemia, or multiple myeloma have reported variable effects of bortezomib on MAPK signaling [[340], [341], [342]], underscoring the context-dependent nature of this interaction.”
From HIF inhibition: Current strategies and clinical challenges (2026) · cites this paper as [341]
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Research works printed but not linked: 14
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Befani, C. D., Vlachostergios, P. J., Hatzidaki, E., Patrikidou, A., Bonanou, S., Simos, G., Papandreou, C. N., & Liakos, P. (2012) · Journal of Molecular Medicine · doi:10.1007/s00109-011-0805-8 · Cited by 135
HIF inhibition: Current strategies and clinical challenges
Więch-Walów, A., Bartoszewska, S., Barton, A., Czechowicz, P., Dudzik, J., Wielockx, B., Collawn, J. F., & Bartoszewski, R. (2026) · Redox biology · doi:10.1016/j.redox.2026.104220 · Cited by 3
Metadata
- Authors
- Esparís‐Ogando, A., Alegre, A., Aguado, B., Mateo, G., Gutiérrez, N., Bladé, J., Schenkein, D., Pandiella, A., & San Miguel, J. F.
- Affiliations
- Hospital Universitario de La Princesa (ES)
- Centro de Investigación del Cáncer (ES)
- Hospital Clínic de Barcelona (ES)
- Takeda Oncology (United States) (US)
- Venue
- International Journal of Cancer
- Publisher
- Wiley
- Published
- 2004-12-17
- Volume
- 114
- Issue
- 4
- Pages
- 665-667
- ISSN
- 0020-7136 (ISSN-L)
- 1097-0215
- OpenAlex
- W2055744416
- Cited by
- 70
- References
- 0
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 7 · 2020: 3 · 2019: 3 · 2018: 3 · 2017: 2 · 2016: 7 · 2015: 1 · 2014: 2 · 2013: 2 · 2012: 3
- FWCI
- 2.75
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Cancer (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Spanish Association Against Cancer
- International Myeloma Foundation
- Fondo de Investigaciones Sanitarias (01/1060)
- Spanish Myeloma Network Program
- Topics
- Health Sciences › Medicine › Hematology › Multiple Myeloma Research and Treatments
- Health Sciences › Medicine › Hematology › Chronic Lymphocytic Leukemia Research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Keywords
- bortezomib, plasma cell leukemia, proteasome inhibitors, monoclonal gammopathy, ERK signaling, caspase-3, PARP cleavage, apoptosis, dexamethasone, doxorubicin, transfusion independence
- MeSH terms
- Bortezomib, Anemia, Antineoplastic Agents, Boronic Acids, Cell Survival, Female, Humans, Leukemia, Plasma Cell, Middle Aged, Multiple Myeloma, Poly(ADP-ribose) Polymerases, Protease Inhibitors, Pyrazines, Thrombocytopenia, Time Factors, Blotting, Western, Apoptosis, Mitogen-Activated Protein Kinase 1, Caspases, Mitogen-Activated Protein Kinase 3, Cell Proliferation, Caspase 3
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