ReviewTH open : companion journal to thrombosis and haemostasis2018
BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?
Review in TH open : companion journal to thrombosis and haemostasis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 35 citations in OpenAlex.
- Endothelial Injury as a Potential Contributor to Cardiovascular Toxicity in Hematologic Malignancies.Diseases (Basel, Switzerland) · 2026Review
- Distinct endothelial cell toxicities of Abl tyrosine kinase inhibitors lead to arterial thrombosis.Blood vessels, thrombosis & hemostasis · 2026Article
- Cholesterol in hematological malignancies: metabolism, mechanisms, and clinical implications.Frontiers in immunology · 2026Review
- Cardiotoxicity Induced by Anticancer Therapies: A Call for Integrated Cardio-Oncology Practice.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Article
- Secondary malignancies after chronic myeloid leukaemia upon TKI treatment: Population trends and outcomes.British journal of haematology · 2025Article
- Genetic associations of plasma proteins and breast cancer identify potential therapeutic drug candidates.Communications biology · 2025Article
- Tyrosine Kinase Inhibitors as Risk Factors for Cerebral Vascular Disease: Report of Two Cases and Literature Review.Case reports in neurological medicine · 2025Article
- Advancements in Protein Kinase Inhibitors: From Discovery to Clinical Applications.Research (Washington, D.C.) · 2025Review
- Endothelium as a Source of Cardiovascular Toxicity From Antitumor Kinase Inhibitors.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Ponatinib Induces a Procoagulant Phenotype in Human Coronary Endothelial Cells via Inducing Apoptosis.Pharmaceutics · 2024Article
- Synthesis of Novel Nilotinib Analogues and Biological Evaluation of Their Antiplatelet Activity and Functionality towards Cancer Cell Proliferation In Vitro.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Hypertension in Cardio-Oncology Clinic: an update on etiology, assessment, and management.Cardio-oncology (London, England) · 2023Review
- Endothelial function measured by peripheral arterial tonometry in patients with chronic myeloid leukemia on tyrosine kinase inhibitor therapy: a pilot study.Cardio-oncology (London, England) · 2023Article
- Differential vascular endothelial cell toxicity of established and novel BCR-ABL tyrosine kinase inhibitors.PloS one · 2023Article
- ROCK and Rolling Towards Predicting BCR-ABL Kinase Inhibitor-Induced Vascular Toxicity.JACC. CardioOncology · 2022Article
- Prevention of venous thromboembolism in hematologic neoplasms: an expert consensus from SEHH-SETH.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Predictive value of clinical examination parameters for cardiovascular adverse events during treatment of chronic myeloid leukemia with tyrosine kinase inhibitors.International journal of hematology · 2022Article
- Cancer Therapies and Vascular Toxicities.Current treatment options in oncology · 2022Review
- Exploiting polypharmacology to dissect host kinases and kinase inhibitors that modulate endothelial barrier integrity.Cell chemical biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Imatinib, the first-in-class BCR-ABL tyrosine kinase inhibitor (TKI), had been a revolution for the treatment of chronic myeloid leukemia (CML) and had greatly enhanced patient survival. Second- (dasatinib, nilotinib, and bosutinib) and third-generation (ponatinib) TKIs have been developed to be effective against BCR-ABL mutations making imatinib less effective. However, these treatments have been associated with arterial occlusive events. This review gathers clinical data and experiments about the pathophysiology of these arterial occlusive events with BCR-ABL TKIs. Imatinib is associated with very low rates of thrombosis, suggesting a potentially protecting cardiovascular effect of this treatment in patients with BCR-ABL CML. This protective effect might be mediated by decreased platelet secretion and activation, decreased leukocyte recruitment, and anti-inflammatory or antifibrotic effects. Clinical data have guided mechanistic studies toward alteration of platelet functions and atherosclerosis development, which might be secondary to metabolism impairment. Dasatinib, nilotinib, and ponatinib affect endothelial cells and might induce atherogenesis through increased vascular permeability. Nilotinib also impairs platelet functions and induces hyperglycemia and dyslipidemia that might contribute to atherosclerosis development. Description of the pathophysiology of arterial thrombotic events is necessary to implement risk minimization strategies.
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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.