Evidence map›Paper›PMID 33972520›Full record

ArticleNature communications2021

Mutations inhibiting KDM4B drive ALT activation in ATRX-mutated glioblastomas.

M Udugama, L Hii, A Garvie, M Cervini, B Vinod, F-L Chan, P P Das, J R Mann, P Collas, H P J Voon and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 55 citations in OpenAlex.

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  6. CHAMP1 complex promotes heterochromatin assembly and reduces replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

11 authors at 3 institutions in 3 countries.

M Udugama *Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.ORCID 0000-0003-0412-4142
L Hii *Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
A GarvieDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
M CerviniDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
B VinodDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
F-L ChanDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
P P DasDepartment of Anatomy and Developmental Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
J R MannDepartment of Anatomy and Developmental Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
P CollasDepartment of Molecular Medicine, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway.
H P J VoonDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia. joanna.voon@monash.edu.ORCID 0000-0002-7179-6611
L H WongDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia. lee.wong@monash.edu.ORCID 0000-0002-4005-7330
Australian Regenerative Medicine Institute · AUDiscovery Institute · USOslo University Hospital · NO

Funding

Worldwide Cancer Research 21-0146
6 · The paper itself

Abstract

Alternative Lengthening of Telomeres (ALT) is a telomere maintenance pathway utilised in 15% of cancers. ALT cancers are strongly associated with inactivating mutations in ATRX; yet loss of ATRX alone is insufficient to trigger ALT, suggesting that additional cooperating factors are involved. We identify H3.3

Indexed as

AdultAnimalsChromatinChromatin ImmunoprecipitationChromatin Immunoprecipitation SequencingDNA ReplicationEmbryonic Stem CellsGene Knockout TechniquesGlioblastomaHistone DemethylasesHistonesHumansIn Situ Hybridization, FluorescenceIsocitrate DehydrogenaseJumonji Domain-Containing Histone DemethylasesMiceAtrx protein, mouseChromatinHistone DemethylasesHistonesIdh1 protein, mouseIsocitrate Dehydrogenaseisocitrate dehydrogenase 2, mouseJumonji Domain-Containing Histone DemethylasesKDM4B protein, humanKdm4b protein, mouseTelomeraseTert protein, mouseTrp53 protein, mouseTumor Suppressor Protein p53X-linked Nuclear Protein

Identifiers

PMID33972520
PMCPMC8110556
OpenAlexW3162688964

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.