Evidence map›Paper›PMID 28757617›Full record

ArticleLeukemia2017

Nilotinib-induced vasculopathy: identification of vascular endothelial cells as a primary target site.

E Hadzijusufovic, K Albrecht-Schgoer, K Huber, G Hoermann, F Grebien, G Eisenwort, W Schgoer, S Herndlhofer, C Kaun, M Theurl and 10 more

Open access · greenAbstract read
In one paragraph

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
9.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

81 citing papers in PubMed, 151 citations in OpenAlex.

  1. Observational
  2. Article
  3. Vascular Toxicities of Cancer Therapies: 2025 Update.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Navigating the Complexities of Cancer Treatment-Induced Hypertension.Journal of cardiovascular development and disease · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Endothelium as a Source of Cardiovascular Toxicity From Antitumor Kinase Inhibitors.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  15. Article
  16. Article
  17. Review
  18. Nilotinib-Associated Multiple Silent Arterial Stenoses in a Patient with Chronic Myeloid LeukemiaTurkish journal of haematology : official journal of Turkish Society of Haematology · 2024
    Article
  19. Article
  20. Article

21 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 6 institutions in 2 countries.

E HadzijusufovicLudwig Boltzmann Cluster Oncology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0001-7409-4204
K Albrecht-SchgoerDepartment of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.
K HuberResearch Center for Molecular Medicine (CeMM), Vienna, Austria.ORCID 0000-0002-1103-5300
G HoermannDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
F GrebienResearch Center for Molecular Medicine (CeMM), Vienna, Austria.ORCID 0000-0003-4289-2281
G EisenwortLudwig Boltzmann Cluster Oncology, Medical University of Vienna, Vienna, Austria.
W SchgoerDepartment of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.
S HerndlhoferDepartment of Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Vienna, Austria.
C KaunDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Vienna, Austria.
M TheurlDepartment of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.
W R SperrLudwig Boltzmann Cluster Oncology, Medical University of Vienna, Vienna, Austria.
U RixResearch Center for Molecular Medicine (CeMM), Vienna, Austria.ORCID 0000-0002-8242-2770
I SadovnikDepartment of Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Vienna, Austria.
B JilmaDepartment of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria.
G H SchernthanerDepartment of Internal Medicine II, Division of Angiology, Medical University of Vienna, Vienna, Austria.
J WojtaDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Vienna, Austria.
D WolfMedical Clinic 3, Oncology, Hematology and Rheumatology, University Clinic Bonn (UKB), Bonn, Germany.
G Superti-FurgaResearch Center for Molecular Medicine (CeMM), Vienna, Austria.ORCID 0000-0002-0570-1768
R KirchmairDepartment of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.
P ValentLudwig Boltzmann Cluster Oncology, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · ATCeMM Research Center for Molecular Medicine · ATInnsbruck Medical University · ATLudwig Boltzmann Institute for Cardiovascular Research · ATUniversity Hospital Bonn · DEUniversity of Veterinary Medicine Vienna · AT

Funding

Austrian Science Fund FWF F 4701Austrian Science Fund FWF F 4704Austrian Science Fund FWF F 5404Austrian Science Fund FWF F 5412
6 · The paper itself

Abstract

The BCR/ABL1 inhibitor Nilotinib is increasingly used to treat patients with chronic myeloid leukemia (CML). Although otherwise well-tolerated, Nilotinib has been associated with the occurrence of progressive arterial occlusive disease (AOD). Our objective was to determine the exact frequency of AOD and examine in vitro and in vivo effects of Nilotinib and Imatinib on endothelial cells to explain AOD-development. In contrast to Imatinib, Nilotinib was found to upregulate pro-atherogenic adhesion-proteins (ICAM-1, E-selectin, VCAM-1) on human endothelial cells. Nilotinib also suppressed endothelial cell proliferation, migration and tube-formation and bound to a distinct set of target-kinases, relevant to angiogenesis and atherosclerosis, including angiopoietin receptor-1 TEK, ABL-2, JAK1 and MAP-kinases. Nilotinib and siRNA against ABL-2 also suppressed KDR expression. In addition, Nilotinib augmented atherosclerosis in ApoE-/- mice and blocked reperfusion and angiogenesis in a hindlimb-ischemia model of arterial occlusion, whereas Imatinib showed no comparable effects. Clinically overt AOD-events were found to accumulate over time in Nilotinib-treated patients. After a median observation-time of 2.0 years, the AOD-frequency was higher in these patients (29.4%) compared to risk factor- and age-matched controls (<5%). Together, Nilotinib exerts direct pro-atherogenic and anti-angiogenic effects on vascular endothelial cells, which may contribute to development of AOD in patients with CML.

Indexed as

AdultAgedAged, 80 and overAnimalsApolipoproteins EAtherosclerosisEndothelium, VascularFemaleHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedProtein Kinase InhibitorsApolipoproteins EnilotinibProtein Kinase InhibitorsPyrimidines

Identifiers

PMID28757617
PMCPMC5669463
OpenAlexW2740029254

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.