Evidence map›Paper›PMID 25849941›Full record

ArticleOncotarget2015

Transforming growth factor-β pathway activity in glioblastoma.

Karl Frei, Dorothee Gramatzki, Isabel Tritschler, Judith Johanna Schroeder, Larisa Espinoza, Elisabeth Jane Rushing, Michael Weller

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 4 pooled it
5.4field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 4 syntheses or guidelines pooled it, 101 citations in OpenAlex.

  1. Pooled it
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  4. Pooled it
  5. Trial
  6. Trial
  7. Article
  8. Review
  9. Autologous profiling reveals inter-patient heterogeneity in Vδ2Journal for immunotherapy of cancer · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Armored bicistronic CAR T cells with dominant-negative TGF-β receptor II to overcome resistance in glioblastoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  14. Article
  15. Review
  16. Review
  17. Heliyon · 2023
    Article
  18. Article
  19. Article
  20. Review

1 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

7 authors at 2 institutions in 1 country.

Karl FreiDepartment of Neurosurgery, University Hospital Zurich, Zurich, Switzerland.
Dorothee GramatzkiLaboratory for Molecular Neuro-Oncology, Department of Neurology, University Hospital Zurich, Zurich, Switzerland.
Isabel TritschlerLaboratory for Molecular Neuro-Oncology, Department of Neurology, University Hospital Zurich, Zurich, Switzerland.
Judith Johanna SchroederLaboratory for Molecular Neuro-Oncology, Department of Neurology, University Hospital Zurich, Zurich, Switzerland.
Larisa EspinozaDepartment of Neurosurgery, University Hospital Zurich, Zurich, Switzerland.
Elisabeth Jane RushingDepartment of Neuropathology, University Hospital Zurich, Zurich, Switzerland.
Michael WellerLaboratory for Molecular Neuro-Oncology, Department of Neurology, University Hospital Zurich, Zurich, Switzerland.
University Hospital of Zurich · CHUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor (TGF)-β is a central molecule maintaining the malignant phenotype of glioblastoma. Anti-TGF-β strategies are currently being explored in early clinical trials. Yet, there is little contemporary data on the differential expression of TGF-β isoforms at the mRNA and protein level or TGF-β/Smad pathway activity in glioblastomas in vivo.Here we studied 64 newly diagnosed and 16 recurrent glioblastomas for the expression of TGF-β1-3, platelet-derived growth factor (PDGF)-B, and plasminogen activator inhibitor (PAI)-1 mRNA by RT-PCR and for the levels of TGF-β1-3 protein, phosphorylated Smad2 (pSmad2), pSmad1/5/8 and PAI-1 by immunohistochemistry.Among the TGF-β isoforms, TGF-β1 mRNA was the most, whereas TGF-β3 mRNA was the least abundant. TGF-β1-3 mRNA expression was strongly correlated, as was the expression of TGF-β1-3 mRNA, and of the TGF-β1-3 target genes, PDGF-B and PAI-1. TGF-β2 and TGF-β3 protein levels correlated well, whereas the comparison of the other TGF-βisoforms did not. Positive correlation was also observed between TGF-β1 and pSmad1/5/8 and between pSmad2 and pSmad1/5/8. Survival analyses indicated that a group of patients with high expression levels of TGF-β2 mRNA or pSmad1/5/8 protein have inferior outcome.We thus provide potential biomarkers for patient stratification in clinical trials of anti-TGF-β therapies in glioblastoma.

Indexed as

AdolescentAdultAgedAged, 80 and overBiomarkers, TumorBrain NeoplasmsCells, CulturedChildChild, PreschoolFemaleGlioblastomaHumansInfantMaleMiddle AgedNeoplasm Recurrence, LocalBiomarkers, TumorTransforming Growth Factor betabiomarkerglioblastomaPAI-1PDGF-BTGF-β

Identifiers

PMID25849941
PMCPMC4467414
OpenAlexW1521384669

What OpenQuestion holds

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LicenceCC BY
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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.