ArticleLeukemia2015
Ibrutinib inhibits collagen-mediated but not ADP-mediated platelet aggregation.
Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 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
100 citing papers in PubMed, 225 citations in OpenAlex.
- A Phase II Trial of the Bruton Tyrosine-Kinase Inhibitor Zanubrutinib (BGB-3111) in Patients with Relapsed/Refractory Waldenström Macroglobulinemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Trial
- Zanubrutinib for the treatment of patients with Waldenström macroglobulinemia: 3 years of follow-up.Blood · 2020Trial
- Trial
- Treatment of relapsed/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma with the BTK inhibitor zanubrutinib: phase 2, single-arm, multicenter study.Journal of hematology & oncology · 2020Trial
- A pilot study of lower doses of ibrutinib in patients with chronic lymphocytic leukemia.Blood · 2018Trial
- Acalabrutinib in relapsed or refractory mantle cell lymphoma (ACE-LY-004): a single-arm, multicentre, phase 2 trial.Lancet (London, England) · 2018Trial
- Trial
- Use of anticoagulants and antiplatelet in patients with chronic lymphocytic leukaemia treated with single-agent ibrutinib.British journal of haematology · 2017Trial
- Incidence and risk factors of bleeding-related adverse events in patients with chronic lymphocytic leukemia treated with ibrutinib.Haematologica · 2015Trial
- Comparison of variably specific Bruton tyrosine kinase inhibitors on platelet aggregation mediated by Fcγ receptor (FcγR) IIa, glycoprotein VI, and platelet endothelial aggregation receptor (PEAR) 1: implications for Bruton tyrosine kinase inhibitors as antithrombotic therapy.Research and practice in thrombosis and haemostasis · 2026Article
- Simulation of perioperative Ibrutinib withdrawal using a population pharmacokinetic model and sparse clinical concentration data.Cancer chemotherapy and pharmacology · 2025Article
- Acute kidney injury after pulsed field ablation in a patient with Waldenström's macroglobulinemia: A case report.HeartRhythm case reports · 2025Article
- Zanubrutinib in the treatment of Waldenström Macroglobulinemia.Future oncology (London, England) · 2025Review
- Article
- Patients with Waldenström macroglobulinemia have impaired platelet and coagulation function.Blood advances · 2024Article
- Targeting Bruton's tyrosine kinase (BTK) as a signaling pathway in immune-mediated diseases: from molecular mechanisms to leading treatments.Advances in rheumatology (London, England) · 2024Review
- NF-kB affects migration of vascular smooth muscle cells after treatment with heparin and ibrutinib.Biochemistry and biophysics reports · 2024Article
- BTK inhibitors in CLL: second-generation drugs and beyond.Blood advances · 2024Review
- Cardiovascular Toxicities of BTK Inhibitors in Chronic Lymphocytic Leukemia:JACC. CardioOncology · 2023Review
- Current concepts and novel targets for antiplatelet therapy.Nature reviews. Cardiology · 2023Review
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 7 institutions in 3 countries.
Funding
Abstract
The BTK (Bruton's tyrosine kinase) inhibitor ibrutinib is associated with an increased risk of bleeding. A previous study reported defects in collagen- and adenosine diphosphate (ADP)-dependent platelet responses when ibrutinib was added ex vivo to patient samples. Whereas the collagen defect is expected given the central role of BTK in glycoprotein VI signaling, the ADP defect lacks a mechanistic explanation. In order to determine the real-life consequences of BTK platelet blockade, we performed light transmission aggregometry in 23 patients receiving ibrutinib treatment. All patients had reductions in collagen-mediated platelet aggregation, with a significant association between the degree of inhibition and the occurrence of clinical bleeding or bruising (P=0.044). This collagen defect was reversible on drug cessation. In contrast to the previous ex vivo report, we found no in vivo ADP defects in subjects receiving standard doses of ibrutinib. These results establish platelet light transmission aggregometry as a method for gauging, at least qualitatively, the severity of platelet impairment in patients receiving ibrutinib treatment.
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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 OpenQuestion graph.