Evidence map›Paper›PMID 29352318›Full record

ArticlePloS one2018

Temozolomide-induced increase of tumorigenicity can be diminished by targeting of mitochondria in in vitro models of patient individual glioblastoma.

Doreen William, Madlin Walther, Björn Schneider, Michael Linnebacher, Carl Friedrich Classen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. {ZnMolecules (Basel, Switzerland) · 2026
    Article
  3. Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025
    Review
  4. Article
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  12. Repurposing FDA approved drugs inhibiting mitochondrial function for targeting glioma-stem like cells.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Article
  13. Article
  14. Review
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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 at 1 institution in 1 country.

Doreen WilliamUniversity Children's and Adolescents' Hospital, University Medicine of Rostock, Rostock, Germany.ORCID 0000-0001-7824-5073
Madlin WaltherUniversity Children's and Adolescents' Hospital, University Medicine of Rostock, Rostock, Germany.
Björn SchneiderInstitute of Pathology, University Medicine of Rostock, Rostock, Germany.
Michael LinnebacherDepartment of Surgery, University Medicine of Rostock, Schillingallee Rostock, Germany.
Carl Friedrich ClassenUniversity Children's and Adolescents' Hospital, University Medicine of Rostock, Rostock, Germany.
University of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is a highly heterogeneous and aggressive brain tumor with a dismal prognosis. Development of resistance towards cytostatic drugs like the GBM standard drug temozolomide is a severe problem in GBM treatment. One potential source of GBM relapse could be so called cancer stem like cells (CSCs). These represent an undifferentiated subpopulation of cells with high potential for tumor initiation. Furthermore, it has been shown that differentiated GBM cells can regain CSC properties when exposed to continuous temozolomide treatment in vitro. In this study, treatment of several primary GBM cell lines with clinically relevant doses of temozolomide increased their tumorigenicity as determined by colony formation assays in soft agar. Increased tumorigenicity is a known property of CSCs. Hence, therapy options that specifically target CSCs are under investigation. CSCs appear to be particularly dependent on mitochondria biogenesis which may represent a useful target for CSC elimination. Toxicity towards mitochondria is a known side effect of several antibiotics. Thus, addition of antibiotics like doxycycline may represent a useful tool to inhibit CSCs in GBM. Here, we show that combining temozolomide treatment of primary GBM cells with doxycycline could counteract the increase of tumorigenicity induced by temozolomide treatment.

Indexed as

Anti-Bacterial AgentsAntineoplastic Agents, AlkylatingBiomarkers, TumorBrain NeoplasmsCell DifferentiationCell Line, TumorDacarbazineDNA Modification MethylasesDNA Repair EnzymesDoxycyclineDrug Resistance, NeoplasmFucosyltransferasesGlioblastomaHumansLewis X AntigenMitochondriaAnti-Bacterial AgentsAntineoplastic Agents, AlkylatingBiomarkers, TumorDacarbazineDNA Modification MethylasesDNA Repair EnzymesDoxycyclineFucosyltransferasesFUT4 protein, humanLewis X AntigenMGMT protein, humanNES protein, humanNestinTemozolomideTumor Suppressor Proteins

Identifiers

PMID29352318
PMCPMC5774812
OpenAlexW2792863726

What OpenQuestion holds

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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.