Evidence map›Paper›PMID 32069807›Full record

ArticleCancers2020

The IL-1 Antagonist Anakinra Attenuates Glioblastoma Aggressiveness by Dampening Tumor-Associated Inflammation.

Max Hübner, David Effinger, Tingting Wu, Gabriele Strauß, Kristin Pogoda, Friedrich-Wilhelm Kreth, Simone Kreth

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Enhanced efficacy of a next-generation EEEV self-replicating RNA platform for combination cancer immunotherapies.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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  9. Dysregulation of inflammasome activation in glioma.Cell communication and signaling : CCS · 2023
    Review
  10. Article
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  13. Article
  14. Review
  15. Article
  16. Review
  17. IL1B-Expressing Exhausted CD4Cancer genomics & proteomics
    Article
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 2 institutions in 1 country.

Max HübnerDepartment of Anesthesiology, University Hospital, LMU Munich, 81377 Munich, Germany.
David EffingerDepartment of Anesthesiology, University Hospital, LMU Munich, 81377 Munich, Germany.
Tingting WuDepartment of Anesthesiology, University Hospital, LMU Munich, 81377 Munich, Germany.
Gabriele StraußDepartment of Anesthesiology, University Hospital, LMU Munich, 81377 Munich, Germany.
Kristin PogodaWalter-Brendel Center of Experimental Medicine, Faculty of Medicine, LMU Munich, 81377 Munich, Germany.
Friedrich-Wilhelm KrethDepartment of Neurosurgery, University Hospital, LMU Munich, 81377 Munich, Germany.
Simone KrethDepartment of Anesthesiology, University Hospital, LMU Munich, 81377 Munich, Germany.
Ludwig-Maximilians-Universität München · DELMU Klinikum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe recombinant IL-1 receptor antagonist anakinra-currently approved for the treatment of autoinflammatory diseases-blocks IL-1β-mediated inflammatory signaling. As inflammation is a major driver of cancer, we hypothesized that anakinra might be able to mitigate glioblastoma (GBM) aggressiveness.

methodsPrimary GBM or T98G cells were incubated alone or with peripheral blood mononuclear cells (PBMCs) and were subsequently treated with IL-1β and/or anakinra. T cells were obtained by magnetic bead isolation. Protein and mRNA expression were quantified by SDS-PAGE, qRT-PCR, and ELISA, respectively. Cell proliferation and apoptosis were analyzed via flow cytometry. Chemotaxis was studied via time-lapse microscopy.

resultsUpon IL-1β stimulation, anakinra attenuated proinflammatory gene expression in both GBM cells and PBMCs, and mitigated tumor migration and proliferation. In a more lifelike model replacing IL-1β stimulation by GBM-PBMC co-culture, sole presence of PBMCs proved sufficient to induce a proinflammatory phenotype in GBM cells with enhanced proliferation and migration rates and attenuated apoptosis. Anakinra antagonized these pro-tumorigenic effects and, moreover, reduced inflammatory signaling in T cells without compromising anti-tumor effector molecules.

conclusionBy dampening the inflammatory crosstalk between GBM and immune cells, anakinra mitigated GBM aggressiveness. Hence, counteracting IL-1β-mediated inflammation might be a promising strategy to pursue.

Indexed as

anakinraglioblastomaIL-1βinflammation

Identifiers

PMID32069807
PMCPMC7072290
OpenAlexW3005716788

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.