Evidence map›Paper›PMID 32567735›Full record

ArticleThe EMBO journal2020

Microglia promote glioblastoma via mTOR-mediated immunosuppression of the tumour microenvironment.

Anaelle A Dumas, Nicola Pomella, Gabriel Rosser, Loredana Guglielmi, Claire Vinel, Thomas O Millner, Jeremy Rees, Natasha Aley, Denise Sheer, Jun Wei and 6 more

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 1 pooled it
12.7field-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

110 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Microglial fructose metabolism is essential for glioblastoma growth.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  11. Review
  12. Review
  13. The Role of Chaf1b in Maintaining Glioma Stem Cell Stemness and Regulating Microglial Polarization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025
    Review
  18. Review
  19. Review
  20. Article

50 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

16 authors at 6 institutions in 3 countries.

Anaelle A DumasBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University London, London, UK.
Nicola PomellaBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University London, London, UK.
Gabriel RosserBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University London, London, UK.
Loredana GuglielmiBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University London, London, UK.
Claire VinelBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University London, London, UK.
Thomas O MillnerBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University London, London, UK.
Jeremy ReesNational Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, London, UK.
Natasha AleyDivision of Neuropathology, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK.
Denise SheerBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University London, London, UK.ORCID 0000-0001-9067-1796
Jun WeiDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Anantha MarisettyDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Amy B HeimbergerDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Robert L BowmanHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Sebastian BrandnerNational Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, London, UK.ORCID 0000-0002-9821-0342
Johanna A JoyceDepartment of Oncology, Ludwig Institute for Cancer Research, University of Lausanne, Lausanne, Switzerland.
Silvia MarinoBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University London, London, UK.ORCID 0000-0002-9612-2883
Queen Mary University of London · GBThe University of Texas MD Anderson Cancer Center · USUniversity College London Hospitals NHS Foundation Trust · GBLudwig Cancer Research · CHMemorial Sloan Kettering Cancer Center · USNational Hospital for Neurology and Neurosurgery · GB

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Medical Research Council G0800020Medical Research Council MR/N000528/1National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/L000954/1NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Tumour-associated microglia/macrophages (TAM) are the most numerous non-neoplastic populations in the tumour microenvironment in glioblastoma multiforme (GBM), the most common malignant brain tumour in adulthood. The mTOR pathway, an important regulator of cell survival/proliferation, is upregulated in GBM, but little is known about the potential role of this pathway in TAM. Here, we show that GBM-initiating cells induce mTOR signalling in the microglia but not bone marrow-derived macrophages in both in vitro and in vivo GBM mouse models. mTOR-dependent regulation of STAT3 and NF-κB activity promotes an immunosuppressive microglial phenotype. This hinders effector T-cell infiltration, proliferation and immune reactivity, thereby contributing to tumour immune evasion and promoting tumour growth in mouse models. The translational value of our results is demonstrated in whole transcriptome datasets of human GBM and in a novel in vitro model, whereby expanded-potential stem cells (EPSC)-derived microglia-like cells are conditioned by syngeneic patient-derived GBM-initiating cells. These results raise the possibility that microglia could be the primary target of mTOR inhibition, rather than the intrinsic tumour cells in GBM.

Indexed as

Immune ToleranceAnimalsBrain NeoplasmsCell Line, TumorGlioblastomaHumansMiceMice, KnockoutMicrogliaNeoplasm ProteinsTOR Serine-Threonine KinasesTumor MicroenvironmentmTOR protein, mouseNeoplasm ProteinsTOR Serine-Threonine KinasesglioblastomamicrogliamTORTAMT cells

Identifiers

PMID32567735
PMCPMC7396846
OpenAlexW3036247540

What OpenQuestion holds

Textmetadata
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.