AI Article Synopsis
- High-risk multiple myeloma patients show poor clinical outcomes compared to standard-risk patients, as identified through cytogenetic and FISH testing.
- A study of 670 myeloma patients revealed that 11% were classified as high-risk, displaying lower response rates and significantly shorter progression-free and overall survival times after undergoing autologous stem-cell transplantation.
- The presence of multiple high-risk cytogenetic abnormalities correlates with worse survival, emphasizing the need for tailored treatment strategies for these patients despite advancements in therapies.
Article Abstract
Background: Conventional cytogenetics and interphase fluorescence in-situ hybridization (FISH) identify a high-risk multiple myeloma population characterized by poor response and short survival.
Patients And Methods: We compared outcomes between high-risk and standard-risk myeloma patients who underwent autologous hematopoietic stem-cell transplantation (auto-HCT) at our institution between January 2005 and December 2009. High-risk myeloma was defined as -13/del(13q) or hypodiploidy in at least 2 metaphases of conventional cytogenetics, or -17/del(17p), t(4;14), t(14;16), t(14;20), hypodiploidy (< 45 chromosomes excluding -Y), or chromosome 1 abnormalities (+1q, -1p, t(1;x)) on FISH or conventional cytogenetics.
Results: Of 670 myeloma patients, 74 (11%) had high-risk myeloma. These high-risk patients had significantly lower overall response rates (74% vs. 85%; P < .01), shorter median progression-free survival (10.3 vs. 32.4 months; P < .001), and shorter overall survival (28 months vs. not reached; P < .001) than the standard-risk patients. Having only 1 high-risk cytogenetic abnormality or experiencing at least very good partial remission after auto-HCT independently predicted improved progression-free survival and overall survival (P < .05) in high-risk patients.
Conclusion: Even in an era of novel therapies, cytogenetically identified high-risk myeloma patients have worse prognoses than standard-risk myeloma patients after auto-HCT, and having more than 1 high-risk cytogenetic abnormality further reduces survival.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4644689 | PMC |
| http://dx.doi.org/10.1016/j.clml.2015.07.641 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Salvage Autologous Transplant in Relapsed Multiple Myeloma: Long-Term Follow-Up of the Phase 3 GMMG ReLApsE Trial.
Blood
January 2025
Universitätsklinikum Heidelberg, Med. Klinik V, GMMG-Studygroup, Heidelberg, Germany.
The multicenter, phase III GMMG ReLApsE trial (EudraCT-No:2009-013856-61) randomized relapsed and/or refractory multiple myeloma (RRMM) patients equally to lenalidomide/dexamethasone (LEN/DEX, 25mg days 1-21/40mg weekly, 4-week cycles) re-induction, salvage high dose chemotherapy (sHDCT, melphalan 200mg/m2), autologous stem cell transplantation (ASCT) and LEN maintenance (10mg/day; transplant arm, n=139) versus continuous LEN/DEX (control arm, n=138). Ninety-four percent of patients had received frontline HDCT/ASCT. We report an updated analysis of survival endpoints with a median follow-up of 99 months.
View Article and Find Full Text PDFEfficacy of bortezomib combined with Hyper-CVAD in adults with relapsed acute lymphoblastic leukemia or positive measurable residual disease; effect of bortezomib in leukemia.
Blood Res
January 2025
Hematology Laboratory, General Hospital of Mexico "Dr. Eduardo Liceaga", Mexico City, Mexico.
Purpose: Despite advances in the treatment of adult acute lymphoblastic leukemia (ALL), relapse remains the most significant challenge in improving prognosis. Measurable residual disease (MRD) assessment can predict bone marrow relapse based on MRD positivity. As access to innovative therapies remains limited because of the high cost, chemotherapy is the widely utilized treatment option.
View Article and Find Full Text PDFBackground: Hemophagocytic lymphohistiocytosis (HLH) is a rare complication of multiple myeloma (MM), with limited data available on its incidence, clinical presentation, and treatment. The underlying mechanisms linking MM and HLH remain unclear, including the potential role of MM treatment agents in triggering HLH.
Methods: This case report presents a patient with MM who developed HLH while on lenalidomide maintenance therapy.
Identification of USP2 as a novel target to induce degradation of KRAS in myeloma cells.
Acta Pharm Sin B
December 2024
Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Chemical Biology Division of Shanghai Universities E-Institutes, Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Inducing the degradation of KRAS represents a novel strategy to combat cancers with KRAS mutation. In this study, we identify ubiquitin-specific protease 2 (USP2) as a novel deubiquitinating enzyme of KRAS in multiple myeloma (MM). Specifically, we demonstrate that gambogic acid (GA) forms a covalent bond with the cysteine 284 residue of USP2 through an allosteric pocket, inhibiting its deubiquitinating activity.
View Article and Find Full Text PDFTargeting deubiquitinase USP7-mediated stabilization of XPO1 contributes to the anti-myeloma effects of selinexor.
J Transl Med
January 2025
Department of Hematology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Background: Targeting exportin1 (XPO1) with Selinexor (SEL) is a promising therapeutic strategy for patients with multiple myeloma (MM). However, intrinsic and acquired drug resistance constitute great challenges. SEL has been reported to promote the degradation of XPO1 protein in tumor cells.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!