Evidence map›Paper›PMID 34381018›Full record

ArticleCell death & disease2021

Alcohol-abuse drug disulfiram targets pediatric glioma via MLL degradation.

Stefanie Meier, Sandra Cantilena, Maria Victoria Niklison Chirou, John Anderson, Darren Hargrave, Paolo Salomoni, Jasper de Boer, David Michod

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Trial
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  3. Case Report: Application ofFrontiers in oncology · 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

8 authors at 3 institutions in 2 countries.

Stefanie MeierCancer Section, Development Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, London, UK.ORCID 0000-0002-2709-8429
Sandra CantilenaCancer Section, Development Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, London, UK.
Maria Victoria Niklison ChirouCentre for Therapeutic Innovation, Department of Pharmacy & Pharmacology, University of Bath, Bath, UK.
John AndersonCancer Section, Development Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, London, UK.ORCID 0000-0001-7509-3203
Darren HargraveCancer Section, Development Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, London, UK.
Paolo SalomoniNuclear Function in CNS Pathophysiology, German Center for Neurodegenerative Diseases, Bonn, Germany.
Jasper de BoerCancer Section, Development Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, London, UK. j.boer@ucl.ac.uk.ORCID 0000-0002-3220-8776
David MichodCancer Section, Development Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, London, UK. d.michod@ucl.ac.uk.ORCID 0000-0002-4187-405X
Great Ormond Street Hospital · GBGerman Center for Neurodegenerative Diseases · DEUniversity of Bath · GB

Funding

Brain Tumour Charity BTC 8/197
6 · The paper itself

Abstract

Pediatric gliomas comprise a broad range of brain tumors derived from glial cells. While high-grade gliomas are often resistant to therapy and associated with a poor outcome, children with low-grade gliomas face a better prognosis. However, the treatment of low-grade gliomas is often associated with severe long-term adverse effects. This shows that there is a strong need for improved treatment approaches. Here, we highlight the potential for repurposing disulfiram to treat pediatric gliomas. Disulfiram is a drug used to support the treatment of chronic alcoholism and was found to be effective against diverse cancer types in preclinical studies. Our results show that disulfiram efficiently kills pediatric glioma cell lines as well as patient-derived glioma stem cells. We propose a novel mechanism of action to explain disulfiram's anti-oncogenic activities by providing evidence that disulfiram induces the degradation of the oncoprotein MLL. Our results further reveal that disulfiram treatment and MLL downregulation induce similar responses at the level of histone modifications and gene expression, further strengthening that MLL is a key target of the drug and explaining its anti-oncogenic properties.

Indexed as

ProteolysisAlcoholismAuranofinCell Line, TumorCell ProliferationChildDisulfiramDown-RegulationDrug RepositioningDrug SynergismGene Expression Regulation, NeoplasticGliomaHistone-Lysine N-MethyltransferaseHistonesHumansLysineAuranofinDisulfiramHistone-Lysine N-MethyltransferaseHistonesKMT2A protein, humanLysineMyeloid-Lymphoid Leukemia Protein

Identifiers

PMID34381018
PMCPMC8358054
OpenAlexW3192219796

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.