Blood
Hematology and Bone Marrow Transplantation Unit, Institute of Medical Pathology, University of Parma, Italy.
Published: July 2003
Patients with multiple myeloma (MM) have increased bone marrow (BM) angiogenesis; however, the proangiogenic properties of myeloma cells and the mechanisms of MM-induced angiogenesis are not completely clarified. The angiopoietin system has been identified as critical in the regulation of vessel formation. In this study we have demonstrated that myeloma cells express several proangiogenic factors, and, in particular, we found that angiopoietin-1 (Ang-1), but not its antagonist Ang-2, was expressed by several human myeloma cell lines (HMCLs) at the mRNA and the protein levels. In a transwell coculture system, we observed that myeloma cells up-regulated the Ang-1 receptor Tie2 in human BM endothelial cells. Moreover, in an experimental model of angiogenesis, the conditioned medium of HMCLs significantly stimulated vessel formation compared with control or vascular endothelial growth factor (VEGF) treatment. The presence of anti-Tie2 blocking antibody completely blunted the proangiogenic effect of XG-6. Finally, our in vitro results were supported by the in vivo finding of Ang-1, but not Ang-2, mRNA and protein expression in purified MM cells obtained from approximately 47% of patients and by high BM angiogenesis in patients with MM positive for Ang-1, suggesting that the angiopoietin system could be involved, at least in part, in MM-induced angiogenesis.
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http://dx.doi.org/10.1182/blood-2002-10-3257 | DOI Listing |
Leukemia
January 2025
UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, CA, USA.
T-cell redirecting therapy (TCRT), specifically chimeric antigen receptor T-cell therapy (CAR T-cells) and bispecific T-cell engagers (TCEs) represent a remarkable advance in the treatment of multiple myeloma (MM). There are several products available around the world and several more in development targeting primarily B-cell maturation antigen (BCMA) and G protein-coupled receptor class C group 5 member D (GRPC5D). The relatively rapid availability of multiple immunotherapies brings the necessity to understand how a certain agent may affect the safety and efficacy of a subsequent immunotherapy so MM physicians and patients can aim at optimal sequential use of these therapies.
View Article and Find Full Text PDFSci Data
January 2025
Federal University of Bahia, Institute of Computing, Salvador, 40170-110, Brazil.
Multiple Myeloma (MM) is a cytogenetically heterogeneous clonal plasma cell proliferative disease whose diagnosis is supported by analyses on histological slides of bone marrow aspirate. In summary, experts use a labor-intensive methodology to compute the ratio between plasma cells and non-plasma cells. Therefore, the key aspect of the methodology is identifying these cells, which relies on the experts' attention and experience.
View Article and Find Full Text PDFClinics (Sao Paulo)
January 2025
Department of Hematology, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, PR China. Electronic address:
Background: The common drugs used for the treatment of Newly Diagnosed Multiple Myeloma (NDMM) include bortezomib and lenalidomide, but the adverse effects of lenalidomide cannot be ignored, especially when it is used in the initial therapy.
Methods: This retrospective study evaluated the efficacy and safety of a modified DVD regimen (pegylated liposomal doxorubicin, bortezomib, and dexamethasone) followed by lenalidomide in the treatment of NDMM. A total of 40 NDMM patients were treated with a reduced dose of pegylated liposomal doxorubicin (20 mg/m) on day 1, subcutaneous bortezomib (1.
Multiple myeloma is characterized by malignant cells which produce high amounts of monoclonal immunoglobulin. Myeloma cells are, therefore, dependent on effective protein degradation. Proteasomal protein degradation is targeted by proteasome inhibitors in routine care.
View Article and Find Full Text PDFEJHaem
February 2025
Department of Laboratory Medicine Hematology Section Clinical Center, NIH Bethesda Maryland USA.
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