ArticleLeukemia2017
Genetic characterization of MYD88-mutated lymphoplasmacytic lymphoma in comparison with MYD88-mutated chronic lymphocytic leukemia.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- MYD88 variants in chronic lymphocytic leukemia exhibit distinct biological behaviors and prognostic implications.Leukemia · 2026Article
- Next-Generation Integrated Sequencing Identifies Poor Prognostic Factors in Patients with MYD88-Mutated Chronic Lymphocytic Leukemia in Taiwan.Pathobiology : journal of immunopathology, molecular and cellular biology · 2025Article
- Genetic and Clinical Characteristics of Korean Chronic Lymphocytic Leukemia Patients with High Frequencies ofInternational journal of molecular sciences · 2023Article
- Nucleic Acid Biomarkers in Waldenström Macroglobulinemia and IgM-MGUS: Current Insights and Clinical Relevance.Diagnostics (Basel, Switzerland) · 2022Review
- MYD88 in the driver's seat of B-cell lymphomagenesis: from molecular mechanisms to clinical implications.Haematologica · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MYD88 (myeloid differentiation primary response 88) is mutated in the majority of Waldenström macroglobulinemia/lymphoplasmacytic lymphoma (LPL); but also, albeit less frequently, in other B-cell malignancies, including chronic lymphocytic leukemia (CLL). This suggests MYD88 as a central regulator of pathogenesis, but requests a broader approach to define diagnostically relevant genetic profiles for LPL and CLL. We identified the L265P hotspot mutation in 86% (n=67/78) of our LPL and 2% (n=12/767) of our CLL cohort. Importantly, in CLL (n=5), but also in LPL (n=4) other MYD88 mutations were identified. MYD88-mutated LPL was characterized by CXCR4 mutations (25%) and del(6q) (19%), whereas both aberrations were absent in the MYD88-unmutated LPL cases. MYD88-mutated CLL formed a prognostically favorable subset with a high frequency of del(13q), mutated IGHV status and no adverse aberrations (del(11q), del(17p), TP53 mutations). MYD88-mutated CLL differed from LPL with respect to cytogenetic aberrations and the absence of CXCR4 mutations. In both entities, based on mutation load evaluation, MYD88 mutations were found to be present in the stem clone in each case, whereas CXCR4 (LPL) and SF3B1 (CLL) mutations also occurred in subclones only.
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