Evidence map›Paper›PMID 25632305›Full record

ArticleGenome medicine2015

TET proteins and the control of cytosine demethylation in cancer.

Laurianne Scourzic, Enguerran Mouly, Olivier A Bernard

Open access · goldAbstract read
In one paragraph

Article in Genome medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed
12.4field-weighted citation impact, top 1% 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

119 citing papers in PubMed, 241 citations in OpenAlex.

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  7. HemaSphere · 2026
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  17. Glutamine is critical for the maintenance of type 1 conventional dendritic cells in normal tissue and the tumor microenvironment.Proceedings of the National Academy of Sciences of the United States of America · 2024
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59 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Laurianne ScourzicInstitut National de la Santé et de la Recherche Médicale (INSERM), Unité 1170, équipe labellisée Ligue Contre le Cancer, 94805 Villejuif, France ; Institut Gustave Roussy, 94805 Villejuif, France ; University Paris 11 Sud, 91405 Orsay, France.
Enguerran MoulyInstitut National de la Santé et de la Recherche Médicale (INSERM), Unité 1170, équipe labellisée Ligue Contre le Cancer, 94805 Villejuif, France ; Institut Gustave Roussy, 94805 Villejuif, France ; University Paris 11 Sud, 91405 Orsay, France.
Olivier A BernardInstitut National de la Santé et de la Recherche Médicale (INSERM), Unité 1170, équipe labellisée Ligue Contre le Cancer, 94805 Villejuif, France ; Institut Gustave Roussy, 94805 Villejuif, France ; University Paris 11 Sud, 91405 Orsay, France.
Institut Gustave Roussy · FRLa Ligue Contre le Cancer · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The discovery that ten-eleven translocation (TET) proteins are α-ketoglutarate-dependent dioxygenases involved in the conversion of 5-methylcytosines (5-mC) to 5-hydroxymethylcytosine (5-hmC), 5-formylcytosine and 5-carboxycytosine has revealed new pathways in the cytosine methylation and demethylation process. The description of inactivating mutations in TET2 suggests that cellular transformation is in part caused by the deregulation of this 5-mC conversion. The direct and indirect deregulation of methylation control through mutations in DNA methyltransferase and isocitrate dehydrogenase (IDH) genes, respectively, along with the importance of cytosine methylation in the control of normal and malignant cellular differentiation have provided a conceptual framework for understanding the early steps in cancer development. Here, we review recent advances in our understanding of the cytosine methylation cycle and its implication in cellular transformation, with an emphasis on TET enzymes and 5-hmC. Ongoing clinical trials targeting the activity of mutated IDH enzymes provide a proof of principle that DNA methylation is targetable, and will trigger further therapeutic applications aimed at controlling both early and late stages of cancer development.

Identifiers

PMID25632305
PMCPMC4308928
OpenAlexW2147734470

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.