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Introduction: Chromosome 1q copy gains (with-1q-gain) is a frequently observed genetic abnormality in multiple myeloma (MM) patients. Recent research has demonstrated that 1q gain is a prognostic factor, linked to poorer clinical outcomes.
Methods: This study was conducted at the Princess Margaret Cancer Centre to examine the clinical outcomes of newly diagnosed MM patients' with-1q-gain or without-1q-gain abnormality. The study included 275 patients, with 161 (58.5%) with-1q-gain abnormality. The median follow-up time for the cohort was 94.3 months (95% CI 30.1-38.6).
Results: The patients' with-1q-gain when compared to without-1q-gain were more likely to have other high-risk cytogenetic abnormalities (34.8% vs. 14.0%, < 0.001) and more advanced disease according to the International Staging System (ISS III, < 0.014). Furthermore, a relatively higher proportion of with-1q-gain patients received tandem autologous stem cell transplant (ASCT) as frontline therapy (36.2% vs. 8.7%, ≤ 0.001).To assess the impact of 1q copy number, patients with 3 copies of 1q (1q-gain3) were compared to those with ≥4 copies (1q-Amp). No significant differences were observed between the two groups.
Conclusion: In conclusion, our study provides insight into the clinical significance of 1q gain abnormality in MM patients at a single center, and highlights its association with adverse prognostic features and treatment outcomes.
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http://dx.doi.org/10.1002/jha2.70045 | DOI Listing |
Anticancer Drugs
September 2025
Department of Blood and Marrow Transplantation, Tianjin Cancer Hospital Airport Hospital, National Clinical Research Center for Cancer.
Bortezomib resistance in multiple myeloma (MM) is a significant clinical challenge that limits the long-term effectiveness. Currently, there is a lack of reliable biomarkers to predict bortezomib resistance. Previous studies reported that several proteins regulate bortezomib resistance through targeting ubiquitin-proteasome pathways, including heat shock protein family A member 9 (HSPA9), dickkopf Wnt signaling pathway inhibitor 1 (DKK1), proteasome 26S subunit non-ATPase 14 (PSMD14), and tripartite motif containing 21 (TRIM21).
View Article and Find Full Text PDFBMB Rep
September 2025
Basic Research Laboratory, Department of Physiology, College of Medicine, Smart Marine Therapeutic Center, Cardiovascular and Metabolic Disease Core Research Center, Inje University, Busan 47392, Korea; Department of Health Science and Technology, College of Medicine, Inje University, Busan 47392, K
Patients with multiple myeloma develop resistance to thalidomide during therapy, and the mechanisms to counteract thalidomide resistance remain elusive. Here, we explored the interaction between cereblon and mitochondrial function to mitigate thalidomide resistance in multiple myeloma. Measurements of cell viability, ATP production, mitochondrial membrane potential, mitochondrial ROS, and protein expression via western blotting were conducted in vitro using KSM20 and KMS26 cells to assess the impact of thalidomide on multiple myeloma.
View Article and Find Full Text PDFEur J Haematol
September 2025
Department of Translational Biomedicine and Neuroscience, University of Bari, Bari, Italy.
In 1994, Vacca, Ribatti, and colleagues demonstrated for the first time that bone marrow microvascular density was significantly increased in multiple myeloma (MM) compared to monoclonal gammopathies of undetermined significance (MGUS) and moreover in active vs. non-active forms. Starting from 1994, the aim of this review article is to summarize the most important acquisitions in the literature concerning the role of angiogenesis in MM progression and the possibility to use anti-angiogenic drugs in its treatment.
View Article and Find Full Text PDFBest Pract Res Clin Haematol
September 2025
Department of Hematology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, China. Electronic address:
Multiple myeloma (MM) is a malignant disease in which clonal plasma cells proliferate abnormally. In patients with MM, the number and function of NK cells are suppressed, resulting in reduced immune surveillance and clearance of myeloma cells. Restoring or enhancing the killing effect of NK cells on myeloma cells is an important strategy for MM immunotherapy.
View Article and Find Full Text PDFBest Pract Res Clin Haematol
September 2025
Department of Personalized Medicine and Rare Diseases, Medfuture Institute for Biomedical Research - Department of Hematology, Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania; Department of Hematology, Ion Chiricuta Cancer Center, Cluj Napoca, Romania. Electronic address:
Plasma cell myeloma (multiple myeloma) is a blood cancer characterized by the clonal proliferation of plasma cells in the bone marrow. Treatment strategies evolve year by year, new drugs getting Food and Drug Administration (FDA)-approved each year. Chimeric antigen receptor (CAR) therapies are an advanced form of immunotherapy that engineer T cells to recognize and destroy cancer cells.
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