Evidence map›Paper›PMID 24498027›Full record

ArticlePloS one2014

The failure in the stabilization of glioblastoma-derived cell lines: spontaneous in vitro senescence as the main culprit.

Ewelina Stoczynska-Fidelus, Sylwester Piaskowski, Michal Bienkowski, Mateusz Banaszczyk, Krystyna Hulas-Bigoszewska, Marta Winiecka-Klimek, Anna Radomiak-Zaluska, Waldemar Och, Maciej Borowiec, Jolanta Zieba and 2 more

Abstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

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  12. EGFRJournal of oncology · 2019
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  19. Different mutational characteristics of TSG in cell lines and surgical specimens.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    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

12 authors.

Ewelina Stoczynska-FidelusDepartment of Tumor Biology, Medical University of Lodz, Lodz, Poland.
Sylwester PiaskowskiDepartment of Tumor Biology, Medical University of Lodz, Lodz, Poland.
Michal BienkowskiDepartment of Molecular Pathology and Neuropathology, Chair of Oncology, Medical University of Lodz, Lodz, Poland.
Mateusz BanaszczykDepartment of Tumor Biology, Medical University of Lodz, Lodz, Poland.
Krystyna Hulas-BigoszewskaDepartment of Molecular Pathology and Neuropathology, Chair of Oncology, Medical University of Lodz, Lodz, Poland.
Marta Winiecka-KlimekDepartment of Tumor Biology, Medical University of Lodz, Lodz, Poland.
Anna Radomiak-ZaluskaNeurological Surgery, The Maria Sklodowska-Curie Regional Specialist Hospital in Zgierz, Zgierz, Lodz, Poland.
Waldemar OchClinical Department of Neurosurgery, The Voivodal Specialistic Hospital in Olsztyn, Olsztyn, Warmia and Masuria, Poland.
Maciej BorowiecDepartment of Paediatrics, Oncology, Haematology and Diabetology, Medical University of Lodz, Lodz, Poland.
Jolanta ZiebaDepartment of Tumor Biology, Medical University of Lodz, Lodz, Poland.
Cezary TredaDepartment of Tumor Biology, Medical University of Lodz, Lodz, Poland.
Piotr RieskeDepartment of Tumor Biology, Medical University of Lodz, Lodz, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell line analysis is an important element of cancer research. Despite the progress in glioblastoma cell culturing, the cells isolated from the majority of specimens cannot be propagated infinitely in vitro. The aim of this study was to identify the processes responsible for the stabilization failure. Therefore, we analyzed 56 primary GB cultures, 7 of which were stabilized. Our results indicate that senescence is primarily responsible for the glioblastoma cell line stabilization failure, while mitotic catastrophe and apoptosis play a minor role. Moreover, a new technical approach allowed for a more profound analysis of the senescent cells in primary cultures, including the distinction between tumor and normal cells. In addition, we observed that glioblastoma cells in primary cultures have a varied potential to undergo spontaneous in vitro senescence, which is often higher than that of the normal cells infiltrating the tumor. Thus, this is the first report of GB cells in primary cell cultures (including both monolayer and spheroid conditions) rapidly and spontaneously becoming senescent. Intriguingly, our data also suggest that nearly half of GB cell lines have a combination of TP53 mutation and CDKN2A homozygous deletion, which are considered as mutually exclusive in glioblastoma. Moreover, recognition of the mechanisms of senescence and mitotic catastrophe in glioblastoma cells may be a step towards a potential new therapeutic approach.

Indexed as

ApoptosisBase SequenceBrain NeoplasmsCell Line, TumorCell MovementCellular SenescenceCyclin-Dependent Kinase Inhibitor p16DNA Mutational AnalysisGene DeletionGlioblastomaHumansMitosisMolecular Sequence DataMutationNeoplastic Stem CellsTumor Suppressor Protein p53Cyclin-Dependent Kinase Inhibitor p16TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24498027
PMCPMC3910690

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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.