This is the authors' abstract. We don't add key points for this paper.
Background Multiple myeloma (MM) is a genetically heterogeneous malignancy in which cytogenetic abnormalities critically influence prognosis. The prognostic significance of 17p gain/amplification (17p+), particularly relative to del(17p) and the high‐risk 1q21 gain/amplification (1q21+), remains insufficiently defined. Methods We retrospectively analyzed 125 MM patients treated at a single center between 2015 and 2024. Cytogenetic profiles were assessed using fluorescence in situ hybridization (FISH). Kaplan–Meier curves and Cox proportional hazards models evaluated the impact of 17p+ on progression‐free survival 1 (PFS1), time to next treatment (TTNT), and overall survival (OS). Results Compared with del(17p), 17p+ was associated with significantly longer PFS1 (HR 0.21, p < 0.01), TTNT (HR 0.18, p < 0.01), and OS (HR 0.25, p < 0.05). In patients receiving proteasome inhibitor–based therapy or not undergoing autologous stem cell transplantation, 17p+ remained favorable for PFS1 (HR 0.20, p < 0.05, HR 0.21, p < 0.01). Multivariate Cox models confirmed 17p+ as an independent protective factor for PFS1 (HR 0.08), TTNT (HR 0.07), and OS (HR 0.02) (all p < 0.001). Among patients with 1q21+, co‐occurrence of 17p+ improved PFS1 (HR 0.47) and TTNT (HR 0.36) ( p < 0.05), though no significant OS benefit was observed. Conclusions 17p+ is associated with markedly improved clinical outcomes in MM and may partially mitigate the adverse prognostic impact of 1q21+. These findings highlight the relevance of 17p+ in cytogenetic risk stratification and personalized treatment strategies and support further validation in multicenter cohorts. Trial Registration The authors have confirmed clinical trial registration is not needed for this submission.
No takes yet. Share an insight, caveat, or question.
Wang et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: