Evidence map›Paper›PMID 27482885›Full record

Trial reportThe Journal of clinical investigation2016

Dasatinib induces lung vascular toxicity and predisposes to pulmonary hypertension.

Christophe Guignabert, Carole Phan, Andrei Seferian, Alice Huertas, Ly Tu, Raphaël Thuillet, Caroline Sattler, Morane Le Hiress, Yuichi Tamura, Etienne-Marie Jutant and 9 more

Open access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed, 1 pooled it
21.2field-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

138 citing papers in PubMed, 1 synthesis or guideline pooled it, 269 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The right time, the right cell: the potential for precision senotherapy in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Cellular senescence in adult pulmonary hypertension: current state and future challenges.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review

78 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

19 authors at 5 institutions in 1 country.

Christophe Guignabert
Carole Phan
Andrei Seferian
Alice Huertas
Ly Tu
Raphaël Thuillet
Caroline Sattler
Morane Le Hiress
Yuichi Tamura
Etienne-Marie Jutant
Marie-Camille Chaumais
Stéphane Bouchet
Benjamin Manéglier
Mathieu Molimard
Philippe Rousselot
Olivier Sitbon
Gérald Simonneau
David Montani
Marc Humbert
Inserm · FRHôpital Marie Lannelongue · FRCentre Hospitalier de Versailles · FRTechnologie Médicale (France) · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a life-threatening disease that can be induced by dasatinib, a dual Src and BCR-ABL tyrosine kinase inhibitor that is used to treat chronic myelogenous leukemia (CML). Today, key questions remain regarding the mechanisms involved in the long-term development of dasatinib-induced PAH. Here, we demonstrated that chronic dasatinib therapy causes pulmonary endothelial damage in humans and rodents. We found that dasatinib treatment attenuated hypoxic pulmonary vasoconstriction responses and increased susceptibility to experimental pulmonary hypertension (PH) in rats, but these effects were absent in rats treated with imatinib, another BCR-ABL tyrosine kinase inhibitor. Furthermore, dasatinib treatment induced pulmonary endothelial cell apoptosis in a dose-dependent manner, while imatinib did not. Dasatinib treatment mediated endothelial cell dysfunction via increased production of ROS that was independent of Src family kinases. Consistent with these findings, we observed elevations in markers of endothelial dysfunction and vascular damage in the serum of CML patients who were treated with dasatinib, compared with CML patients treated with imatinib. Taken together, our findings indicate that dasatinib causes pulmonary vascular damage, induction of ER stress, and mitochondrial ROS production, which leads to increased susceptibility to PH development.

Indexed as

AdultAnimalsAntineoplastic AgentsApoptosisCells, CulturedDasatinibE-SelectinFemaleGenetic Predisposition to DiseaseHemodynamicsHumansHypertension, PulmonaryHypoxiaImatinib MesylateIntercellular Adhesion Molecule-1Leukemia, Myelogenous, Chronic, BCR-ABL PositiveAntineoplastic AgentsDasatinibE-SelectinImatinib MesylateIntercellular Adhesion Molecule-1Reactive Oxygen SpeciesVascular Cell Adhesion Molecule-1

Identifiers

PMID27482885
PMCPMC5004960
OpenAlexW2496712281

What OpenQuestion holds

Textmetadata
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.