ArticleOncotarget2016
Genetic predisposition and induced pro-inflammatory/pro-oxidative status may play a role in increased atherothrombotic events in nilotinib treated chronic myeloid leukemia patients.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- NETosis and Neutrophil Activity Quantification in Pediatric Patients with Essential Thrombocythemia.International journal of molecular sciences · 2025Article
- Tyrosine Kinase Inhibitors as Risk Factors for Cerebral Vascular Disease: Report of Two Cases and Literature Review.Case reports in neurological medicine · 2025Article
- Pro-Inflammatory Signaling Cascade Markers, Oxidative Stress-Inflammatory Signaling Axis, and Chronic Total Occlusion of Tibial Artery in Elderly Patients Suffering from Occlusion of Coronary Arteries.Current topics in medicinal chemistry · 2024Article
- Concentration of low-density lipoproteins (LDL) is significantly reduced after nilotinib discontinuation.Scientific reports · 2023Observational
- Article
- Cross-Domain Text Mining to Predict Adverse Events from Tyrosine Kinase Inhibitors for Chronic Myeloid Leukemia.Cancers · 2022Article
- Cardioprotection of High-Risk Individuals.Heart failure clinics · 2022Review
- Pro-Inflammatory and Pro-Oxidative Changes During Nilotinib Treatment in CML Patients: Results of a Prospective Multicenter Front-Line TKIs Study (KIARO Study).Frontiers in oncology · 2022Article
- Lifelong TKI therapy: how to manage cardiovascular and other risks.Hematology. American Society of Hematology. Education Program · 2021Review
- The JAK-STAT pathway: an emerging target for cardiovascular disease in rheumatoid arthritis and myeloproliferative neoplasms.European heart journal · 2021Article
- Arterial hypertension assessment in a population with chronic myeloid leukemia.Scientific reports · 2021Observational
- Cardiovascular Issues in Tyrosine Kinase Inhibitors Treatments for Chronic Myeloid Leukemia: A Review.Frontiers in physiology · 2021Review
- Vascular toxic effects of cancer therapies.Nature reviews. Cardiology · 2020Review
- The CoV-2 outbreak: how hematologists could help to fight Covid-19.Pharmacological research · 2020Article
- Peripheral Artery Disease and Stroke.Journal of cardiovascular echography · 2020Review
- Mechanisms of Cardiovascular Toxicity of BCR-ABL1 Tyrosine Kinase Inhibitors in Chronic Myelogenous Leukemia.Current hematologic malignancy reports · 2020Review
- From Molecular Mechanisms to Clinical Management of Antineoplastic Drug-Induced Cardiovascular Toxicity: A Translational Overview.Antioxidants & redox signaling · 2019Review
- Safety and efficacy of nilotinib in routine clinical practice in patients with chronic myeloid leukemia in chronic or accelerated phase with resistance or intolerance to imatinib: results from the NOVEL study.Therapeutic advances in hematology · 2018Article
- The use of the tyrosine kinase inhibitor Nilotinib in Spondyloarthritis: does targeting inflammatory pathways with a treatment lead to vascular toxicity?Journal of translational medicine · 2017Review
- TheOncotarget · 2017Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several reports described an increased risk of cardiovascular (CV) events, mainly atherothrombotic, in Chronic Myeloid Leukemia (CML) patients receiving nilotinib. However, the underlying mechanism remains elusive. The objective of the current cross-sectional retrospective study is to address a potential correlation between Tyrosine Kinase Inhibitors (TKIs) treatment and CV events. One hundred and 10 chronic phase CML patients in complete cytogenetic response during nilotinib or imatinib, were screened for CV events and evaluated for: traditional CV risk factors, pro/anti-inflammatory biochemical parameters and detrimental ORL1 gene polymorphisms (encoding for altered oxidized LDL receptor-1). Multivariate analysis of the whole cohort showed that the cluster of co-existing nilotinib treatment, dyslipidaemia and G allele of LOX-1 polymorphism was the only significant finding associated with CV events. Furthermore, multivariate analysis according to TKI treatment confirmed IVS4-14 G/G LOX-1 polymorphism as the strongest predictive factor for a higher incidence of CV events in nilotinib patients. Biochemical assessment showed an unbalanced pro-inflammatory cytokines network in nilotinib vs imatinib patients. Surprisingly, pre-existing traditional CV risk factors were not always predictive of CV events. We believe that in nilotinib patients an induced "inflammatory/oxidative status", together with a genetic pro-atherothrombotic predisposition, may favour the increased incidence of CV events. Prospective studies focused on this issue are ongoing.
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