Evidence map›Paper›PMID 23625925›Full record

ArticleThe Journal of biological chemistry2013

Reduced immunosuppressive properties of axitinib in comparison with other tyrosine kinase inhibitors.

Franziska Stehle, Kristin Schulz, Corinna Fahldieck, Jana Kalich, Rudolf Lichtenfels, Dagmar Riemann, Barbara Seliger

Registry-linked trialOpen access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04197219 (Pembrolizumab With Axitinib in Recurrent Endometrial Cancer With Deficient Mismatch Repair System Post PD1 Exposure), which is not on this map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 8% 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.

NCT04197219 phase2withdrawnnot on this mapstarted 2021, after this paper: background citation

Pembrolizumab With Axitinib in Recurrent Endometrial Cancer With Deficient Mismatch Repair System Post PD1 Exposure: Phase II Trial

TypeinterventionalSponsorCase Comprehensive Cancer CenterRan2021 to 2026Enrolled0ConditionsRecurrent Endometrial CancerArmsPembrolizumab, Axitinib
3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 58 citations in OpenAlex.

  1. Trial
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  5. Journal of veterinary science · 2024
    Article
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  9. Review
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  11. Article
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  13. Article
  14. Article
  15. The Binary Classification of Protein Kinases.Journal of inflammation research · 2021
    Article
  16. Review
  17. Anti-Proliferative Effect ofMolecules (Basel, Switzerland) · 2020
    Article
  18. Article
  19. Review
  20. Review
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

7 authors at 1 institution in 1 country.

Franziska StehleInstitute of Medical Immunology, Martin Luther University Halle-Wittenberg, 06112 Halle (Saale), Germany.
Kristin SchulzInstitute of Medical Immunology, Martin Luther University Halle-Wittenberg, 06112 Halle (Saale), Germany.
Corinna FahldieckInstitute of Medical Immunology, Martin Luther University Halle-Wittenberg, 06112 Halle (Saale), Germany.
Jana KalichInstitute of Medical Immunology, Martin Luther University Halle-Wittenberg, 06112 Halle (Saale), Germany.
Rudolf LichtenfelsInstitute of Medical Immunology, Martin Luther University Halle-Wittenberg, 06112 Halle (Saale), Germany.
Dagmar RiemannInstitute of Medical Immunology, Martin Luther University Halle-Wittenberg, 06112 Halle (Saale), Germany.
Barbara SeligerInstitute of Medical Immunology, Martin Luther University Halle-Wittenberg, 06112 Halle (Saale), Germany. Electronic address: barbara.seliger@uk-halle.de.
Martin Luther University Halle-Wittenberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The multikinase inhibitors sunitinib, sorafenib, and axitinib have an impact not only on tumor growth and angiogenesis, but also on the activity and function of immune effector cells. In this study, a comparative analysis of the growth inhibitory properties and apoptosis induction potentials of tyrosine kinase inhibitors on T cells was performed. Tyrosine kinase inhibitor treatment resulted in a dramatic decrease in T cell proliferation along with distinct impacts on the cell cycle progression. This was at least partially associated with an enhanced induction of apoptosis although triggered by distinct apoptotic mechanisms. In contrast to sunitinib and sorafenib, axitinib did not affect the mitochondrial membrane potential (Δψm) but resulted in an induction or stabilization of the induced myeloid leukemia cell differentiation protein (Mcl-1), leading to an irreversible arrest in the G2/M cell cycle phase and delayed apoptosis. Furthermore, the sorafenib-mediated suppression of immune effector cells, in particular the reduction of the CD8(+) T cell subset along with the down-regulation of key immune cell markers such as chemokine CC motif receptor 7 (CCR7), CD26, CD69, CD25, and CXCR3, was not observed in axitinib-treated immune effector cells. Therefore, axitinib rather than sorafenib seems to be suitable for implementation in complex treatment regimens of cancer patients including immunotherapy.

Indexed as

Antigens, CDApoptosisAxitinibCD8-Positive T-LymphocytesFemaleG2 Phase Cell Cycle CheckpointsHumansImidazolesImmunosuppressive AgentsIndazolesJurkat CellsMaleMembrane Potential, MitochondrialM Phase Cell Cycle CheckpointsMyeloid Cell Leukemia Sequence 1 ProteinNeoplasmsAntigens, CDAxitinibCCR7 protein, humanCXCR3 protein, humanImidazolesImmunosuppressive AgentsIndazolesMyeloid Cell Leukemia Sequence 1 ProteinProtein Kinase InhibitorsProto-Oncogene Proteins c-bcl-2Receptors, CCR7Receptors, CXCR3ApoptosisAxitinibImmunologyImmunosuppressionImmunotherapySorafenibSunitinibTargeted TherapyT CellTyrosine Kinase Inhibitor

Identifiers

PMID23625925
PMCPMC3675571
OpenAlexW1984984885

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.