ReviewLeukemia research2017
Risk factors and mechanisms contributing to TKI-induced vascular events in patients with CML.
Review in Leukemia research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 67 citations in OpenAlex.
- Analysis of cardiovascular and arteriothrombotic adverse events in chronic-phase CML patients after frontline TKIs.Blood advances · 2019Trial
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- Risks of Retinal Vascular Occlusions with the Systemic Use of Tyrosine Kinase Inhibitors.Ophthalmology. Retina · 2026Article
- Real-world outcomes of ponatinib in heavily pretreated patients with chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia.Annals of hematology · 2026Article
- Kinase Inhibitors for Targeted Cancer Therapy.Current topics in medicinal chemistry · 2026Review
- Cerebrovascular stenosis related to tyrosine kinase inhibitor for chronic myeloid leukemia: two illustrative cases.BMC neurology · 2025Article
- Intersection of Tyrosine Kinase Inhibition and Sepsis-Induced Cardiomyopathy.Case reports in pathology · 2025Article
- Tyrosine Kinase Inhibitors as Risk Factors for Cerebral Vascular Disease: Report of Two Cases and Literature Review.Case reports in neurological medicine · 2025Article
- The new Systematic Coronary Risk Evaluation (SCORE2 and SCORE2-OP) estimates the risk of arterial occlusive events in chronic myeloid leukemia patients treated with nilotinib or ponatinib.Annals of hematology · 2024Article
- Circulating biomarkers for management of cancer therapeutics-related cardiac dysfunction.Cardiovascular research · 2023Review
- Dasatinib/prednisone induction followed by blinatumomab/dasatinib in Ph+ acute lymphoblastic leukemia.Blood advances · 2023Article
- Hypertension in Cancer Survivors: A Review of the Literature and Suggested Approach to Diagnosis and Treatment.Journal of cardiovascular pharmacology · 2022Review
- Article
- Lifelong TKI therapy: how to manage cardiovascular and other risks.Hematology. American Society of Hematology. Education Program · 2021Review
- Tyrosine Kinase Inhibitors and Vascular Adverse Events in Patients with Chronic Myeloid Leukemia: A Population-Based, Propensity Score-Matched Cohort Study.The oncologist · 2021Article
- Arterial hypertension assessment in a population with chronic myeloid leukemia.Scientific reports · 2021Observational
- Visualization of Kinase Inhibition-Related Adverse Events Using the Japanese Adverse Drug Event Report Database.Drugs - real world outcomes · 2021Article
- Etiology and management of hypertension in patients with cancer.Cardio-oncology (London, England) · 2021Review
- Arterial Hypertension and Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia: A Systematic Review and Meta-Analysis.Frontiers in pharmacology · 2021Article
- Cardiovascular Issues in Tyrosine Kinase Inhibitors Treatments for Chronic Myeloid Leukemia: A Review.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Vascular adverse events (VAE) are an emerging problem in patients with chronic myeloid leukemia (CML) receiving second-generation BCR-ABL1 tyrosine kinase inhibitors (TKI). Relevant VAE comprise peripheral, cerebral, and coronary artery changes in patients receiving nilotinib, venous and arterial occlusive events during ponatinib therapy, and pulmonary hypertension in patients receiving dasatinib. Although each TKI binds to a unique profile of molecular targets in leukemic cells and vascular cells, the exact etiology of drug-induced vasculopathies remains uncertain. Recent data suggest that predisposing molecular factors, pre-existing cardiovascular risk factors as well as certain comorbidities contribute to the etiology of VAE in these patients. In addition, direct effects of these TKI on vascular endothelial cells have been demonstrated and are considered to contribute essentially to VAE evolution. In the current article, we discuss mechanisms underlying the occurrence of VAE in TKI-treated patients with CML, with special emphasis on vascular and perivascular target cells and involved molecular (vascular) targets of VAE-triggering TKI. In addition, we discuss optimal patient selection and drug selection through which the risk of occurrence of cardiovascular events can hopefully be minimized while maintaining optimal anti-leukemic effects in CML, thereby following the principles of personalized medicine.
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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.