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December 8, 2025BloodOpen Access

Genetic evolution of Waldenström macroglobulinemia across disease stages

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Authors

SDSurendra DasariMayo Clinic in Florida
Shaji Kumar
Shaji KumarMayo ClinicMBMiles Del BussoMayo Clinic

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Overview

Whole exome sequencing reveals mutational landscape in Waldenström Macroglobulinemia, indicating disease progression patterns.

Key Points

  • To elucidate the mutational profile and genomic landscape of Waldenström Macroglobulinemia across different disease stages.
  • Performed whole exome sequencing on sorted bone marrow aspirates from patients with WM
  • Conducted paired germline sequencing using peripheral blood mononuclear cells
  • Analyzed mutations and copy number variations using advanced genomic techniques
  • Utilized Fisher's exact test for enrichment and hypergeometric test for overlap analyses.
  • 78 high-quality WM samples sequenced showing varied mutational burden across disease stages
  • 77% of samples harbored MYD88L265P mutations
  • Notable alterations in chromatin remodeling genes were observed at relapse
  • Increased frequency of TP53 mutation and copy number variations in RRWM compared to earlier stages.

Cite This Study

Dasari et al. (2025) studied this question.

synapsesocial.com/papers/69362f714fa91c937236e228https://doi.org/10.1182/blood-2025-3540
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Prognostic impact of CXCR4 mutation type on clinical features and outcomes of patients with Waldenström macroglobulinemia2025
  2. 2Prognostic significance of clinical risk models and genomic alterations in Waldenström macroglobulinemia before or after BTK inhibitor era2025
  3. 3P73 | TP53 MUTATION AND MSS-WM IDENTIFY HIGH RISK WALDENSTROM MACROGLOBULINEMIA IN A REAL WORLD COHORT2026
  4. 4MYD88 L265P mutation in Waldenstrom macroglobulinemia2013 · 232 citations
  5. 5LOX1 expression identifies a population of polymorphonuclear myeloid-derived suppressor cells that are highly enriched in bone marrow samples of treatment-Naïve and BTKi-Relapsed/Refractory WM patients and show constitutive activation of BTK2025