Evidence map›Paper›PMID 30292065›Full record

ArticleTranslational oncology2019

Phenotypic and Expressional Heterogeneity in the Invasive Glioma Cells.

Artem Fayzullin, Cecilie J Sandberg, Matthew Spreadbury, Birthe Mikkelsen Saberniak, Zanina Grieg, Erlend Skaga, Iver A Langmoen, Einar O Vik-Mo

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  5. Article
  6. Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024
    Review
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  8. Article
  9. Article
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  18. Article
  19. Tumor Cell Invasion in Glioblastoma.International journal of molecular sciences · 2020
    Review
  20. 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

8 authors at 1 institution in 1 country.

Artem FayzullinVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway. Electronic address: artem.fayzullin@rr-research.no.
Cecilie J SandbergVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway.
Matthew SpreadburyVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway.
Birthe Mikkelsen SaberniakVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway.
Zanina GriegVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway.
Erlend SkagaVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway.
Iver A LangmoenVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway; Department of Neurosurgery, Oslo University Hospital, Oslo, Norway.
Einar O Vik-MoVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway; Department of Neurosurgery, Oslo University Hospital, Oslo, Norway.
Oslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor cell invasion is a hallmark of glioblastoma (GBM) and a major contributing factor for treatment failure, tumor recurrence, and the poor prognosis of GBM. Despite this, our understanding of the molecular machinery that drives invasion is limited.

methodsTime-lapse imaging of patient-derived GBM cell invasion in a 3D collagen gel matrix, analysis of both the cellular invasive phenotype and single cell invasion pattern with microarray expression profiling.

resultsGBM invasion was maintained in a simplified 3D-milieue. Invasion was promoted by the presence of the tumorsphere graft. In the absence of this, the directed migration of cells subsided. The strength of the pro-invasive repulsive signaling was specific for a given patient-derived culture. In the highly invasive GBM cultures, the majority of cells had a neural progenitor-like phenotype, while the less invasive cultures had a higher diversity in cellular phenotypes. Microarray expression analysis of the non-invasive cells from the tumor core displayed a higher GFAP expression and a signature of genes containing VEGFA, hypoxia and chemo-repulsive signals. Cells of the invasive front expressed higher levels of CTGF, TNFRSF12A and genes involved in cell survival, migration and cell cycle pathways. A mesenchymal gene signature was associated with increased invasion.

conclusionThe GBM tumorsphere core promoted invasion, and the invasive front was dominated by a phenotypically defined cell population expressing genes regulating traits found in aggressive cancers. The detected cellular heterogeneity and transcriptional differences between the highly invasive and core cells identifies potential targets for manipulation of GBM invasion.

Identifiers

PMID30292065
PMCPMC6172486
OpenAlexW2895345351

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.