Evidence map›Paper›PMID 40683881›Full record

ArticleNature communications2025

The invasion phenotypes of glioblastoma depend on plastic and reprogrammable cell states.

Milena Doroszko, Rebecka Stockgard, Irem Uppman, Josephine Heinold, Faidra Voukelatou, Hitesh Bhagavanbhai Mangukiya, Thomas O Millner, Madeleine Skeppås, Mar Ballester Bravo, Ramy Elgendy and 8 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Special Issue "Invasion and Metastasis in Brain Cancer".International journal of molecular sciences · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. A Bibenzyl fromAntioxidants (Basel, Switzerland) · 2025
    Article
  14. Article
  15. Downregulation ofFrontiers in oncology · 2025
    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

18 authors.

Milena Doroszko *Department of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.
Rebecka Stockgard *Department of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.
Irem UppmanDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.ORCID http://orcid.org/0000-0003-3602-5544
Josephine HeinoldDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.
Faidra VoukelatouDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.ORCID http://orcid.org/0009-0007-4281-3041
Hitesh Bhagavanbhai MangukiyaDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.ORCID http://orcid.org/0000-0002-8460-4850
Thomas O MillnerBrain Tumour Research Centre, Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London, UK.
Madeleine SkeppåsDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.ORCID http://orcid.org/0009-0003-3741-4143
Mar Ballester BravoDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.
Ramy ElgendyDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.ORCID http://orcid.org/0000-0002-2592-3448
Maria BerglundDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.
Ludmila ElfinehDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.
Cecilia KronaDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.
Soumi KunduDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.ORCID http://orcid.org/0000-0002-0759-3051
Katarzyna KoltowskaDepartment of Immunology, Genetics and Pathology, Uppsala University, Beijer Gene and Neuro Laboratory, Uppsala, Sweden.ORCID http://orcid.org/0000-0002-6841-8900
Silvia MarinoBrain Tumour Research Centre, Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London, UK.ORCID http://orcid.org/0000-0002-9612-2883
Ida LarssonDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden.ORCID http://orcid.org/0000-0001-5422-4243
Sven NelanderDepartment of Immunology, Genetics and Pathology, Uppsala University, Program for Neurooncology and Neurodegeneration, Uppsala, Sweden. sven.nelander@igp.uu.se.ORCID http://orcid.org/0000-0003-1758-1262

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most common primary brain cancer. It causes death mainly by local invasion via several routes, including infiltration of white matter tracts and penetration of perivascular spaces. However, the pathways that mediate these invasion routes are only partly known. Here, we conduct an integrative study to identify cell states and central drivers of route-specific invasion in GBM. Combining single-cell profiling and spatial protein detection in patient-derived xenograft models and clinical tumor samples, we demonstrate a close association between the differentiation state of GBM cells and their choice of invasion route. Computational modeling identifies ANXA1 as a driver of perivascular involvement in GBM cells with mesenchymal differentiation and the transcription factors RFX4 and HOPX as orchestrators of growth and differentiation in diffusely invading GBM cells. Ablation of these targets in tumor cells alters their invasion route, redistributes the cell states, and extends survival in xenografted mice. Our results define a close association between GBM cell differentiation states and invasion routes, identify functional biomarkers of route-specific invasion, and point toward targeted modulation of specific invasive cell states as a therapeutic strategy in GBM.

Indexed as

Brain NeoplasmsGlioblastomaAnimalsCell DifferentiationCell Line, TumorDNA-Binding ProteinsGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansMiceNeoplasm InvasivenessPhenotypeSingle-Cell AnalysisTranscription FactorsDNA-Binding ProteinsHomeodomain ProteinsTranscription Factors

Identifiers

PMID40683881
PMCPMC12276355

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.