ArticleBlood cancer discovery2021
Aberrant Extrafollicular B Cells, Immune Dysfunction, Myeloid Inflammation, and MyD88-Mutant Progenitors Precede Waldenstrom Macroglobulinemia.
Article in Blood cancer discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Clonotypic characterization defines B-cell drivers of clonal expansion and intratumor heterogeneity in IgM monoclonal gammopathies.HemaSphere · 2026Article
- WNK2 oncogenicity revealed by the discovery and functional characterization of novel gene isoforms in MYD88 mutated Waldenström's Macroglobulinemia.Blood cancer journal · 2026Article
- Decoding Waldenström Macroglobulinemia Through Genomics, Epigenomics and Cellular Interactions.International journal of molecular sciences · 2026Review
- Genetically driven immune microenvironment states associate with therapeutic responses in MYD88 mutant lymphomas.Molecular cancer · 2026Article
- The Direction of Modern Therapies in Waldenström Macroglobulinaemia.Journal of cellular and molecular medicine · 2025Review
- Uncovering regulatory B-cell features associated with regulatory T-cell expansion and global T-cell exhaustion in Waldenström macroglobulinemiaHemaSphere · 2025Article
- Review
- Single-cell RNA sequencing defines distinct disease subtypes and reveals hypo-responsiveness to interferon in asymptomatic Waldenstrom's Macroglobulinemia.Nature communications · 2025Article
- Genomic and immune profiling of prognostic risk groups in IgM gammopathy reveals novel biomarkers beyondFrontiers in immunology · 2025Article
- Expanded tumor-associated polymorphonuclear myeloid-derived suppressor cells in Waldenstrom macroglobulinemia display immune suppressive activity.Blood cancer journal · 2024Article
- Personalized neoantigen vaccines as early intervention in untreated patients with lymphoplasmacytic lymphoma: a non-randomized phase 1 trial.Nature communications · 2024Article
- Clonal architecture and evolutionary history of Waldenström's macroglobulinemia at the single-cell level.Disease models & mechanisms · 2023Article
- Dysfunctions of innate and adaptive immune tumor microenvironment in Waldenström macroglobulinemia.International journal of cancer · 2023Article
- Waldenström macroglobulinemia whole genome reveals prolonged germinal center activity and late copy number aberrations.Blood advances · 2023Article
- Impaired SARS-CoV-2 Variant Neutralization and CD8+ T-cell Responses Following 3 Doses of mRNA Vaccines in Myeloma: Correlation with Breakthrough Infections.Blood cancer discovery · 2023Article
- The immune system in multiple myeloma and precursor states: Lessons and implications for immunotherapy and interception.American journal of hematology · 2023Review
- Prognostic impact of MYD88 and CXCR4 mutations assessed by droplet digital polymerase chain reaction in IgM monoclonal gammopathy of undetermined significance and smouldering Waldenström macroglobulinaemia.British journal of haematology · 2023Article
- Single-cell profiles reveal tumor cell heterogeneity and immunosuppressive microenvironment in Waldenström macroglobulinemia.Journal of translational medicine · 2022Article
- Changes in Bone Marrow Tumor and Immune Cells Correlate with Durability of Remissions Following BCMA CAR T Therapy in Myeloma.Blood cancer discovery · 2022Article
- The Landscape of Nucleic-Acid-Based Aptamers for Treatment of Hematologic Malignancies: Challenges and Future Directions.Bioengineering (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Waldenstrom macroglobulinemia (WM) and its precursor IgM gammopathy are distinct disorders characterized by clonal mature IgM-expressing B-cell outgrowth in the bone marrow. Here, we show by high-dimensional single-cell immunogenomic profiling of patient samples that these disorders originate in the setting of global B-cell compartment alterations, characterized by expansion of genomically aberrant extrafollicular B cells of the nonmalignant clonotype. Alterations in the immune microenvironment preceding malignant clonal expansion include myeloid inflammation and naïve B- and T-cell depletion. Host response to these early lesions involves clone-specific T-cell immunity that may include MYD88 mutation-specific responses. Hematopoietic progenitors carry the oncogenic MYD88 mutations characteristic of the malignant WM clone. These data support a model for WM pathogenesis wherein oncogenic alterations and signaling in progenitors, myeloid inflammation, and global alterations in extrafollicular B cells create the milieu promoting extranodal pattern of growth in differentiated malignant cells. SIGNIFICANCE: These data provide evidence that growth of the malignant clone in WM is preceded by expansion of extrafollicular B cells, myeloid inflammation, and immune dysfunction in the preneoplastic phase. These changes may be related in part to MYD88 oncogenic signaling in pre-B progenitor cells and suggest a novel model for WM pathogenesis.
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