ArticleDisease models & mechanisms2023
Clonal architecture and evolutionary history of Waldenström's macroglobulinemia at the single-cell level.
Article in Disease models & mechanisms, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Quantitative MYD88 L265P and flow cytometry levels for outcome determination in IgM gammopathies: the SAL-TO study.Blood advances · 2026Article
- Decoding Waldenström Macroglobulinemia Through Genomics, Epigenomics and Cellular Interactions.International journal of molecular sciences · 2026Review
- Cardiac light chain amyloidosis secondary to Waldenström's macroglobulinemia: A case report and review.Experimental and therapeutic medicine · 2025Article
- Genomic and immune profiling of prognostic risk groups in IgM gammopathy reveals novel biomarkers beyondFrontiers in immunology · 2025Article
- Base excision repair and double strand break repair cooperate to modulate the formation of unrepaired double strand breaks in mouse brain.Nature communications · 2024Article
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
Abstract
To provide insight into the subclonal architecture and co-dependency patterns of the alterations in Waldenström's macroglobulinemia (WM), we performed single-cell mutational and protein profiling of eight patients. A custom panel was designed to screen for mutations and copy number alterations at the single-cell level in samples taken from patients at diagnosis (n=5) or at disease progression (n=3). Results showed that in asymptomatic WM at diagnosis, MYD88L265P was the predominant clonal alteration; other events, if present, were secondary and subclonal to MYD88L265P. In symptomatic WM, clonal diversity was more evident, uncovering combinations of alterations that synergized to promote clonal expansion and dominance. At disease progression, a dominant clone was observed, sometimes accompanied by other less complex minor clones, which could be consistent with a clonal selection process. Clonal diversity was also reduced, probably due to the effect of treatment. Finally, we combined protein expression with mutational analysis to map somatic genotype with the immunophenotype. Our findings provide a comprehensive view of the clonality of tumor populations in WM and how clonal complexity can evolve and impact disease progression.
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Registered trials
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