Evidence map›Paper›PMID 29462414›Full record

ArticleNeuro-oncology2018

Primary glioblastoma cells for precision medicine: a quantitative portrait of genomic (in)stability during the first 30 passages.

Sathishkumar Baskaran, Markus Mayrhofer, Hanna Göransson Kultima, Tobias Bergström, Lioudmila Elfineh, Lucia Cavelier, Anders Isaksson, Sven Nelander

Open access · hybridAbstract read
In one paragraph

Article in Neuro-oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  15. Genomic and Phenotypic Characterization of a Broad Panel of Patient-Derived Xenografts Reflects the Diversity of Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
  16. 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

8 authors at 2 institutions in 1 country.

Sathishkumar BaskaranDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Sweden.
Markus MayrhoferScience for Life Laboratory, Department of Medical Sciences, Uppsala University, Sweden.
Hanna Göransson KultimaScience for Life Laboratory, Department of Medical Sciences, Uppsala University, Sweden.
Tobias BergströmDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Sweden.
Lioudmila ElfinehDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Sweden.
Lucia CavelierDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Sweden.
Anders IsakssonScience for Life Laboratory, Department of Medical Sciences, Uppsala University, Sweden.
Sven NelanderDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Sweden.
Uppsala University · SEScience for Life Laboratory · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Primary glioblastoma cell (GC) cultures have emerged as a key model in brain tumor research, with the potential to uncover patient-specific differences in therapy response. However, there is limited quantitative information about the stability of such cells during the initial 20-30 passages of culture. Methods: We interrogated 3 patient-derived GC cultures at dense time intervals during the first 30 passages of culture. Combining state-of-the-art signal processing methods with a mathematical model of growth, we estimated clonal composition, rates of change, affected pathways, and correlations between altered gene dosage and transcription. Results: We demonstrate that GC cultures undergo sequential clonal takeovers, observed through variable proportions of specific subchromosomal lesions, variations in aneuploid cell content, and variations in subpopulation cell cycling times. The GC cultures also show significant transcriptional drift in several metabolic and signaling pathways, including ribosomal synthesis, telomere packaging and signaling via the mammalian target of rapamycin, Wnt, and interferon pathways, to a high degree explained by changes in gene dosage. In addition to these adaptations, the cultured GCs showed signs of shifting transcriptional subtype. Compared with chromosomal aberrations and gene expression, DNA methylations remained comparatively stable during passaging, and may be favorable as a biomarker. Conclusion: Taken together, GC cultures undergo significant genomic and transcriptional changes that need to be considered in functional experiments and biomarker studies that involve primary glioblastoma cells.

Indexed as

Chromosome AberrationsGenomic InstabilityPrecision MedicineAgedBrain NeoplasmsCell Culture TechniquesCell ProliferationDNA MethylationFemaleGlioblastomaHumansMaleMiddle AgedTumor Cells, Cultured

Identifiers

PMID29462414
PMCPMC6280139
OpenAlexW2793292822

What OpenQuestion holds

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LicenceCC BY-NC
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.