ArticleBlood2024
How I use genomics and BTK inhibitors in the treatment of Waldenström macroglobulinemia.
Article in Blood, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Integrated bioinformatics and clinical validation of oxidative stress-associated genes in atrial fibrillation and chronic kidney disease.Experimental and therapeutic medicine · 2026Article
- Recent advances of dual PROTACs for potential therapeutic applications.Molecular diversity · 2026Review
- 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
- Quantitative MYD88L265P and CXCR4S338X analysis to assess clinical trial performance in Waldenstrom macroglobulinemia.Blood advances · 2026Article
- Physiological distribution and dosimetry of AlBMC medical imaging · 2026Article
- Generational safety profiles of BTK inhibitors: adverse reaction signals and real-world evidence from the FAERS database.Frontiers in medicine · 2026Article
- Bing-Neel Syndrome in Waldenström Macroglobulinemia: Updates on Clinical Management and BTK Inhibitor Efficacy.Cancers · 2025Review
- A Rare Case of Waldenström Macroglobulinemia Presenting as Bilateral Bloody Pleural Effusion and Pancytopenia.The American journal of case reports · 2025Article
- Article
- Investigation of the mechanism of hypertension caused by BTKi in the treatment of hematologic diseases.Frontiers in pharmacology · 2025Review
- Waldenström Macroglobulinemia and Chronic Myelomonocytic Leukemia: Case Report and Literature Review.OncoTargets and therapy · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
abstractMutations in MYD88 (95%-97%) and CXCR4 (30%-40%) are common in Waldenström macroglobulinemia (WM). TP53 is altered in 20% to 30% of patients with WM, particularly those previously treated. Mutated MYD88 activates hematopoietic cell kinase that drives Bruton tyrosine kinase (BTK) prosurvival signaling. Both nonsense and frameshift CXCR4 mutations occur in WM. Nonsense variants show greater resistance to BTK inhibitors. Covalent BTK inhibitors (cBTKi) produce major responses in 70% to 80% of patients with WM. MYD88 and CXCR4 mutation status can affect time to major response, depth of response, and/or progression-free survival (PFS) in patients with WM treated with cBTKi. The cBTKi zanubrutinib shows greater response activity and/or improved PFS in patients with WM with wild-type MYD88, mutated CXCR4, or altered TP53. Risks for adverse events, including atrial fibrillation, bleeding diathesis, and neutropenia can differ based on which BTKi is used in WM. Intolerance is also common with cBTKi, and dose reduction or switchover to another cBTKi can be considered. For patients with acquired resistance to cBTKis, newer options include pirtobrutinib or venetoclax. Combinations of BTKis with chemoimmunotherapy, CXCR4, and BCL2 antagonists are discussed. Algorithms for positioning BTKis in treatment naïve or previously treated patients with WM, based on genomics, disease characteristics, and comorbidities, are presented.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.