Evidence map›Paper›PMID 32779022›Full record

ArticleJournal of cancer research and clinical oncology2020

DNA CpG methylation in sequential glioblastoma specimens.

Zoltan Kraboth, Bence Galik, Marton Tompa, Bela Kajtar, Peter Urban, Attila Gyenesei, Attila Miseta, Bernadette Kalman

Open access · hybridAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  5. ß-Adrenoreceptors in Human Cancers.International journal of molecular sciences · 2023
    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 2 countries.

Zoltan KrabothInstitute of Laboratory Medicine, School of Medicine, University of Pecs, Pecs, Hungary.ORCID http://orcid.org/0000-0003-1661-2653
Bence GalikSzentagothai Research Center, University of Pecs, 20. Ifjusag street, Pecs, 7624, Hungary.ORCID http://orcid.org/0000-0003-1464-3034
Marton TompaInstitute of Laboratory Medicine, School of Medicine, University of Pecs, Pecs, Hungary.ORCID http://orcid.org/0000-0002-4045-6219
Bela KajtarInstitute of Pathology, School of Medicine, University of Pecs, Pecs, Hungary.ORCID http://orcid.org/0000-0001-5551-3709
Peter UrbanSzentagothai Research Center, University of Pecs, 20. Ifjusag street, Pecs, 7624, Hungary.ORCID http://orcid.org/0000-0003-4043-3428
Attila GyeneseiSzentagothai Research Center, University of Pecs, 20. Ifjusag street, Pecs, 7624, Hungary.ORCID http://orcid.org/0000-0003-2925-9342
Attila MisetaInstitute of Laboratory Medicine, School of Medicine, University of Pecs, Pecs, Hungary.ORCID http://orcid.org/0000-0002-7984-3347
Bernadette KalmanInstitute of Laboratory Medicine, School of Medicine, University of Pecs, Pecs, Hungary. Bernadette.kalman@pte.hu.ORCID http://orcid.org/0000-0003-2592-3939
University of Pecs · HUMedical University of Białystok · PL

Funding

Általános Orvostudományi Kar, Pécsi Tudományegyetem Szolcsányi Fund KA-2019-42Elixir Converge 871075H2020 Marie Skłodowska-Curie Actions 754432
6 · The paper itself

Abstract

purposeGlioblastoma is the most aggressive form of brain tumors. A better understanding of the molecular mechanisms leading to its evolution is essential for the development of treatments more effective than the available modalities. Here, we aim to identify molecular drivers of glioblastoma development and recurrence by analyzing DNA CpG methylation patterns in sequential samples.

methodsDNA was isolated from 22 pairs of primary and recurrent formalin-fixed, paraffin-embedded glioblastoma specimens, and subjected to reduced representation bisulfite sequencing. Bioinformatic analyses were conducted to identify differentially methylated sites and pathways, and biostatistics was used to test correlations among clinical and pathological parameters.

resultsDifferentially methylated pathways likely involved in primary tumor development included those of neuronal differentiation, myelination, metabolic processes, synapse organization and endothelial cell proliferation, while pathways differentially active during glioblastoma recurrence involved those associated with cell processes and differentiation, immune response, Wnt regulation and catecholamine secretion and transport.

conclusionDNA CpG methylation analyses in sequential clinical specimens revealed hypomethylation in certain pathways such as neuronal tissue development and angiogenesis likely involved in early tumor development and growth, while suggested altered regulation in catecholamine secretion and transport, Wnt expression and immune response contributing to glioblastoma recurrence. These pathways merit further investigations and may represent novel therapeutic targets.

Indexed as

AdultAgedBrain NeoplasmsCpG IslandsDNA MethylationFemaleGlioblastomaHumansMaleMiddle AgedDNA CpG methylationGene ontology analysesGlioblastomaProgressionTumorigenesis

Identifiers

PMID32779022
PMCPMC7519911
OpenAlexW3048181545

What OpenQuestion holds

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LicenceCC BY
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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.