Evidence map›Paper›PMID 20113470›Full record

ArticleMolecular cancer2010

Effects of nilotinib on regulatory T cells: the dose matters.

Fei Fei, Yingzhe Yu, Anita Schmitt, Markus T Rojewski, Baoan Chen, Jochen Greiner, Marlies Götz, Donald Bunjes, Michael Schmitt

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

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  11. Therapeutic immune monitoring of CD4Oncology letters · 2017
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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

9 authors at 3 institutions in 2 countries.

Fei FeiDepartment of Internal Medicine III, University of Ulm, 89081 Ulm, Germany.
Yingzhe Yu
Anita Schmitt
Markus T Rojewski
Baoan Chen
Jochen Greiner
Marlies Götz
Donald Bunjes
Michael Schmitt
Universität Ulm · DEImmungenetics (Germany) · DEZhongda Hospital Southeast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNilotinib is a tyrosine kinase inhibitor with high target specificity. Here, we characterized the effects of nilotinib for the first time on CD4+CD25+ regulatory T cells (Tregs) which regulate anti-tumor/leukemia immune responses. DESIGN AND

methodsCarboxyfluorescein diacetate succinimidyl ester (CFSE) and 5-bromo-2-deoxy -uridine (BrdU) were used to assess the proliferation and cell cycle distribution of Tregs. The expression of the transcription factor forkhead box P3 (FoxP3) and the glucocorticoid-induced tumor necrosis factor receptor (GITR) were measured by flow cytometry. Western blotting analysis was used to detect the effects of nilotinib on the signal transduction cascade of T-cell receptor (TCR) in Tregs.

resultsNilotinib inhibited the proliferation and suppressive capacity of Tregs in a dose-dependent manner. However, the production of cytokines secreted by Tregs and CD4+CD25- T cells was only inhibited at high concentrations of nilotinib exceeding the mean therapeutic serum concentrations of the drug in patients. Only high doses of nilotinib arrested both Tregs and CD4+CD25- T cells in the G0/G1 phase and down-regulated the expression of FoxP3 and GITR. In western blotting analysis, nilotinib did not show significant inhibitory effects on TCR signaling events in Tregs and CD4+CD25- T cells.

conclusionsThese findings indicate that nilotinib does not hamper the function of Tregs at clinical relevant doses, while long-term administration of nilotinib still needs to be investigated.

Indexed as

ApoptosisCell ProliferationCytokinesDose-Response Relationship, DrugDown-RegulationForkhead Transcription FactorsG1 PhaseGlucocorticoid-Induced TNFR-Related ProteinHumansImmunosuppression TherapyInterleukin-2 Receptor alpha SubunitPyrimidinesReceptors, Antigen, T-CellReceptors, Nerve Growth FactorReceptors, Tumor Necrosis FactorResting Phase, Cell CycleCytokinesForkhead Transcription FactorsFOXP3 protein, humanGlucocorticoid-Induced TNFR-Related ProteinInterleukin-2 Receptor alpha SubunitnilotinibPyrimidinesReceptors, Antigen, T-CellReceptors, Nerve Growth FactorReceptors, Tumor Necrosis FactorTNFRSF18 protein, human

Identifiers

PMID20113470
PMCPMC2835656
OpenAlexW2155493075

What OpenQuestion holds

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LicenceCC BY
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.