ArticleLeukemia2016
Clonal B cells in Waldenström's macroglobulinemia exhibit functional features of chronic active B-cell receptor signaling.
Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Zanubrutinib for the treatment of MYD88 wild-type Waldenström macroglobulinemia: a substudy of the phase 3 ASPEN trial.Blood advances · 2020Trial
- WNK2 oncogenicity revealed by the discovery and functional characterization of novel gene isoforms in MYD88 mutated Waldenström's Macroglobulinemia.Blood cancer journal · 2026Article
- Comprehensive Characterization of Bruton's Tyrosine Kinase Inhibitor Specificity, Potency, and Biological Effects: Insights into Covalent and Noncovalent Mechanistic Signatures.ACS pharmacology & translational science · 2025Review
- Personalized neoantigen vaccines as early intervention in untreated patients with lymphoplasmacytic lymphoma: a non-randomized phase 1 trial.Nature communications · 2024Article
- Waldenström Macroglobulinemia - A State-of-the-Art Review: Part 1: Epidemiology, Pathogenesis, Clinicopathologic Characteristics, Differential Diagnosis, Risk Stratification, and Clinical Problems.Mediterranean journal of hematology and infectious diseases · 2024Review
- Clonal architecture and evolutionary history of Waldenström's macroglobulinemia at the single-cell level.Disease models & mechanisms · 2023Article
- IRAK-4 inhibition: emavusertib for the treatment of lymphoid and myeloid malignancies.Frontiers in immunology · 2023Review
- Current Status of Novel Agents for the Treatment of B Cell Malignancies: What's Coming Next?Cancers · 2022Review
- A new role for the SRC family kinase HCK as a driver of SYK activation in MYD88 mutated lymphomas.Blood advances · 2022Article
- Review
- Successful treatment with tirabrutinib for relapsed lymphoplasmacytic lymphoma complicated by Bing-Neel syndrome.International journal of hematology · 2022Article
- Differential Diagnosis of Waldenström's Macroglobulinemia and Early Management: Perspectives from Clinical Practice.Blood and lymphatic cancer : targets and therapy · 2022Review
- Article
- Resistance Mutations to BTK Inhibitors Originate From the NF-κB but Not From the PI3K-RAS-MAPK Arm of the B Cell Receptor Signaling Pathway.Frontiers in immunology · 2021Review
- Mechanisms of B Cell Receptor Activation and Responses to B Cell Receptor Inhibitors in B Cell Malignancies.Cancers · 2020Review
- Genomic Landscape of Waldenström Macroglobulinemia and Its Impact on Treatment Strategies.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2020Review
- Novel Treatment Strategies in the Management of Waldenström Macroglobulinemia.Current hematologic malignancy reports · 2020Review
- SYK is activated by mutated MYD88 and drives pro-survival signaling in MYD88 driven B-cell lymphomas.Blood cancer journal · 2020Article
- Human MYD88L265P is insufficient by itself to drive neoplastic transformation in mature mouse B cells.Blood advances · 2019Article
- Dimerization of an aptamer generated from Ligand-guided selection (LIGS) yields a high affinity scaffold against B-cells.Biochimica et biophysica acta. General subjects · 2019Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Waldenström's macroglobulinemia (WM) is a B-cell non-Hodgkin's lymphoma (B-NHL) characterized by immunoglobulin M (IgM) monoclonal gammopathy and the medullary expansion of clonal lymphoplasmacytic cells. Neoplastic transformation has been partially attributed to hyperactive MYD88 signaling, secondary to the MYD88 L265P mutation, occurring in the majority of WM patients. Nevertheless, the presence of chronic active B-cell receptor (BCR) signaling, a feature of multiple IgM+ B-NHL, remains a subject of speculation in WM. Here, we interrogated the BCR signaling capacity of primary WM cells by utilizing multiparametric phosphoflow cytometry and found heightened basal phosphorylation of BCR-related signaling proteins, and augmented phosphoresponses on surface IgM (sIgM) crosslinking, compared with normal B cells. In support of those findings we observed high sIgM expression and loss of phosphatase activity in WM cells, which could both lead to signaling potentiation in clonal cells. Finally, led by the high-signaling heterogeneity among WM samples, we generated patient-specific phosphosignatures, which subclassified patients into a 'high' and a 'healthy-like' signaling group, with the second corresponding to patients with a more indolent clinical phenotype. These findings support the presence of chronic active BCR signaling in WM while providing a link between differential BCR signaling utilization and distinct clinical WM subgroups.
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