Evidence map›Paper›PMID 41146055›Full record

ArticleBMC cancer2025

Drug resistant glioblastoma stem cells exhibit enriched stemness signatures and share extracellular matrix overexpression.

Lance L Estabillo, Erlend Skaga, Skarphedinn Halldorsson, Einar O Vik-Mo, Cecilie J Sandberg

Abstract read
In one paragraph

Article in BMC cancer, 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. Review
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

5 authors.

Lance L EstabilloVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research and Department of Neurosurgery, Oslo University Hospital, Oslo, Norway. lance_estabillo@yahoo.com.
Erlend SkagaVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research and Department of Neurosurgery, Oslo University Hospital, Oslo, Norway.
Skarphedinn HalldorssonVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research and Department of Neurosurgery, Oslo University Hospital, Oslo, Norway.
Einar O Vik-MoVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research and Department of Neurosurgery, Oslo University Hospital, Oslo, Norway.
Cecilie J SandbergVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research and Department of Neurosurgery, Oslo University Hospital, Oslo, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUnderstanding the complex molecular mechanisms driving drug resistance in glioblastoma (GBM) is crucial to develop effective therapeutic strategies. While prior studies have identified resistance mechanisms tied to specific drugs or pathways, a multi-modal molecular analysis of resistance across a range of drug classes is lacking.

methodsWe identified highly drug-resistant (n = 5) and drug-sensitive (n = 4) cultures from a cohort of 32 patient-derived glioblastoma stem cell (GSC) cultures screened against a broad panel of ~ 500 anti-cancer drugs. To elucidate the key drivers of drug resistance, we performed integrative profiling of stemness, differentiation capacity, global gene expression, mutation profiles, and DNA methylation patterns between the two groups.

resultsDespite heterogeneous gene expression profiles, drug-resistant GSCs showed consistent upregulation of ATP-binding cassette (ABC) drug efflux transporters, stemness, and extracellular matrix (ECM)-related genes. Compared to drug-sensitive GSCs, drug-resistant GSCs exhibited more pronounced stem-like properties and reduced differentiation capacity. Notably, genes linked to axonogenesis displayed significant CpG island hypomethylation in drug-resistant GSCs.

conclusionsThis study suggests a pivotal role for GSC plasticity, stemness maintenance, and ECM-mediated drug evasion in GBM treatment resistance. Our findings highlight the adaptive and dynamic nature of resistance mechanisms in GSCs, emphasizing the need for comprehensive molecular insights to inform targeted therapeutic strategies in GBM.

Indexed as

Brain NeoplasmsDrug Resistance, NeoplasmExtracellular MatrixGlioblastomaNeoplastic Stem CellsAntineoplastic AgentsCell DifferentiationDNA MethylationGene Expression ProfilingGene Expression Regulation, NeoplasticHumansAntineoplastic AgentsBrain cancerDrug resistanceDrug sensitivityExtracellular matrixGlioblastomaGlioblastoma stem cellsIndividualized medicineResistance mechanismsStemness

Identifiers

PMID41146055
PMCPMC12560458

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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.