Evidence map›Paper›PMID 41070610›Full record

ArticleMolecular medicine reports2025

Glioma‑associated microglia and macrophages as a potential target for mTOR inhibition in glioblastoma.

Pia S Zeiner, Michael Schulz, Jana Schomber, Jan-Béla Weinem, Nadja I Lorenz, Benedikt Sauer, Bastian Roller, Katharina J Weber, Anna-Luisa Luger, Annemarie Berger and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

16 authors.

Pia S ZeinerDr. Senckenberg Institute of Neurooncology, University Hospital, Goethe University Frankfurt, D‑60596 Frankfurt, Germany.
Michael SchulzGeorg‑Speyer‑Haus, Institute for Tumor Biology and Experimental Therapy, D‑60596 Frankfurt, Germany.
Jana SchomberDr. Senckenberg Institute of Neurooncology, University Hospital, Goethe University Frankfurt, D‑60596 Frankfurt, Germany.
Jan-Béla WeinemDr. Senckenberg Institute of Neurooncology, University Hospital, Goethe University Frankfurt, D‑60596 Frankfurt, Germany.
Nadja I LorenzDr. Senckenberg Institute of Neurooncology, University Hospital, Goethe University Frankfurt, D‑60596 Frankfurt, Germany.
Benedikt SauerDr. Senckenberg Institute of Neurooncology, University Hospital, Goethe University Frankfurt, D‑60596 Frankfurt, Germany.
Bastian RollerDr. Senckenberg Institute of Neurooncology, University Hospital, Goethe University Frankfurt, D‑60596 Frankfurt, Germany.
Katharina J WeberFrankfurt Cancer Institute, Goethe University Frankfurt, D‑60596 Frankfurt am Main, Germany.
Anna-Luisa LugerDr. Senckenberg Institute of Neurooncology, University Hospital, Goethe University Frankfurt, D‑60596 Frankfurt, Germany.
Annemarie BergerInstitute for Medical Virology, University Hospital, Goethe University Frankfurt, D‑60596 Frankfurt, Germany.
Karl H PlateFrankfurt Cancer Institute, Goethe University Frankfurt, D‑60596 Frankfurt am Main, Germany.
Lisa SevenichFrankfurt Cancer Institute, Goethe University Frankfurt, D‑60596 Frankfurt am Main, Germany.
Joachim P SteinbachDr. Senckenberg Institute of Neurooncology, University Hospital, Goethe University Frankfurt, D‑60596 Frankfurt, Germany.
Mohammed H MosaFrankfurt Cancer Institute, Goethe University Frankfurt, D‑60596 Frankfurt am Main, Germany.
Patrick N HarterInstitute of Neurology (Edinger‑Institute), University Hospital, Goethe University Frankfurt, D‑60528 Frankfurt, Germany.
Michael W RonellenfitschDr. Senckenberg Institute of Neurooncology, University Hospital, Goethe University Frankfurt, D‑60596 Frankfurt, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma‑associated microglia/macrophages (GAM) constitute the predominant immune cell population in glioblastoma (GB). Both GB cells and GAM exhibit upregulated mTOR signaling. The present study aimed to investigate the effects of pharmacological mTOR inhibition (mTORi) specifically on GAM. The effects of mTORi on signal transduction, cell growth and viability were analyzed in immortalized microglia cell lines. Additionally, a comprehensive analysis of the GAM phenotype was conducted, including whole transcriptome analyses and cytokine profiling. Effects were investigated in a tumor cell/GAM co‑culture model under mTORi with rapamycin or torin2 or treatment with temozolomide, the standard chemotherapy agent for patients with GB. In the

Indexed as

Brain NeoplasmsGlioblastomaMacrophagesMicrogliaMTOR InhibitorsTOR Serine-Threonine KinasesCell Line, TumorCell ProliferationCell SurvivalCoculture TechniquesCytokinesHumansSignal TransductionSirolimusTemozolomideCytokinesMTOR InhibitorsMTOR protein, humanSirolimusTemozolomideTOR Serine-Threonine KinasesgliomamicrogliamTORrapamycintumor microenvironment

Identifiers

PMID41070610
PMCPMC12529088

What OpenQuestion holds

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Registered trials

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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.