Evidence map›Paper›PMID 33673490›Full record

ArticlePharmaceuticals (Basel, Switzerland)2021

Inhibition of Intercellular Cytosolic Traffic via Gap Junctions Reinforces Lomustine-Induced Toxicity in Glioblastoma Independent of MGMT Promoter Methylation Status.

Matthias Schneider, Anna-Laura Potthoff, Bernd O Evert, Marius Dicks, Denise Ehrentraut, Andreas Dolf, Elena N C Schmidt, Niklas Schäfer, Valeri Borger, Torsten Pietsch and 7 more

Open access · goldAbstract read
In one paragraph

Article in Pharmaceuticals (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

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  7. Innovative Therapeutic Strategies Targeting the Network Architecture of Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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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

17 authors at 2 institutions in 1 country.

Matthias SchneiderDepartment of Neurosurgery, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0002-6025-7479
Anna-Laura PotthoffDepartment of Neurosurgery, University Hospital Bonn, 53127 Bonn, Germany.
Bernd O EvertDepartment of Neurology, University Hospital Bonn, 53127 Bonn, Germany.
Marius DicksDepartment of Neurosurgery, University Hospital Bonn, 53127 Bonn, Germany.
Denise EhrentrautDepartment of Neurosurgery, University Hospital Bonn, 53127 Bonn, Germany.
Andreas DolfInstitute of Experimental Immunology, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0001-7264-9456
Elena N C SchmidtDepartment of Neurosurgery, University Hospital Bonn, 53127 Bonn, Germany.
Niklas SchäferBrain Tumor Translational Research Affiliation, University Hospital Bonn, 53127 Bonn, Germany.
Valeri BorgerDepartment of Neurosurgery, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0002-5905-4121
Torsten PietschDepartment of Neuropathology, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0003-0763-6506
Mike-Andrew WesthoffDepartment of Pediatrics and Adolescent Medicine, University Medical Center Ulm, 89075 Ulm, Germany.ORCID 0000-0003-3256-7100
Erdem GüresirDepartment of Neurosurgery, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0001-8319-0847
Andreas WahaBrain Tumor Translational Research Affiliation, University Hospital Bonn, 53127 Bonn, Germany.
Hartmut VatterDepartment of Neurosurgery, University Hospital Bonn, 53127 Bonn, Germany.
Dieter H HeilandTranslational NeuroOncology Research Group, Medical Center University of Freiburg, 79106 Freiburg, Germany.ORCID 0000-0002-9258-3033
Patrick SchussDepartment of Neurosurgery, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0002-5806-2576
Ulrich HerrlingerBrain Tumor Translational Research Affiliation, University Hospital Bonn, 53127 Bonn, Germany.
University Hospital Bonn · DEUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma is a malignant brain tumor and one of the most lethal cancers in human. Temozolomide constitutes the standard chemotherapeutic agent, but only shows limited efficacy in glioblastoma patients with unmethylated O-6-methylguanine-DNA methyltransferase (MGMT) promoter status. Recently, it has been shown that glioblastoma cells communicate via particular ion-channels-so-called gap junctions. Interestingly, inhibition of these ion channels has been reported to render MGMT promoter-methylated glioblastoma cells more susceptible for a therapy with temozolomide. However, given the percentage of about 65% of glioblastoma patients with an unmethylated MGMT promoter methylation status, this treatment strategy is limited to only a minority of glioblastoma patients. In the present study we show that-in contrast to temozolomide-pharmacological inhibition of intercellular cytosolic traffic via gap junctions reinforces the antitumoral effects of chemotherapeutic agent lomustine, independent of MGMT promoter methylation status. In view of the growing interest of lomustine in glioblastoma first and second line therapy, these findings might provide a clinically-feasible way to profoundly augment chemotherapeutic effects for all glioblastoma patients.

Indexed as

gap junctionsglioblastomaintercellular cytosolic trafficlomustinemeclofenamate

Identifiers

PMID33673490
PMCPMC7997332
OpenAlexW3134977520

What OpenQuestion holds

Textmetadata
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.