Evidence map›Paper›PMID 23863747›Full record

SynthesisNature communications2013

Meta-analysis of IDH-mutant cancers identifies EBF1 as an interaction partner for TET2.

Paul Guilhamon, Malihe Eskandarpour, Dina Halai, Gareth A Wilson, Andrew Feber, Andrew E Teschendorff, Valenti Gomez, Alexander Hergovich, Roberto Tirabosco, M Fernanda Amary and 5 more

Open access · hybridAbstract readMeta-Analysis
In one paragraph

Synthesis in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

100 citing papers in PubMed, 179 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Selective Estrogen Receptor Modulators' (SERMs) Influence onInternational journal of molecular sciences · 2024
    Article
  10. Clinico-Genomic Profiling of Conventional and Dedifferentiated Chondrosarcomas Reveals TP53 Mutation to Be Associated with Worse Outcomes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  11. Review
  12. Article
  13. Cancers · 2023
    Review
  14. Review
  15. YBX1-interacting small RNAs andJournal of bone oncology · 2023
    Article
  16. Article
  17. Epigenetic Abnormalities in Chondrosarcoma.International journal of molecular sciences · 2023
    Review
  18. Article
  19. Article
  20. Mechanisms that regulate the activities of TET proteins.Cellular and molecular life sciences : CMLS · 2022
    Review

40 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

15 authors at 5 institutions in 2 countries.

Paul GuilhamonMedical Genomics, UCL Cancer Institute, University College London, London, UK.
Malihe Eskandarpour
Dina Halai
Gareth A Wilson
Andrew Feber
Andrew E Teschendorff
Valenti Gomez
Alexander Hergovich
Roberto Tirabosco
M Fernanda Amary
Daniel Baumhoer
Gernot Jundt
Mark T Ross
Adrienne M Flanagan
Stephan Beck
University College London · GBRoyal National Orthopaedic Hospital NHS Trust · GBUniversity Hospital of Basel · CHIllumina (United Kingdom) · GBLondon Cancer · GB

Funding

Medical Research Council G1000411Wellcome Trust 084071Wellcome Trust 090090Wellcome Trust 090090/Z/09/ZWellcome Trust 99148Worldwide Cancer Research 11-0634
6 · The paper itself

Abstract

Isocitrate dehydrogenase (IDH) genes 1 and 2 are frequently mutated in acute myeloid leukaemia (AML), low-grade glioma, cholangiocarcinoma (CC) and chondrosarcoma (CS). For AML, low-grade glioma and CC, mutant IDH status is associated with a DNA hypermethylation phenotype, implicating altered epigenome dynamics in the aetiology of these cancers. Here we show that the IDH variants in CS are also associated with a hypermethylation phenotype and display increased production of the oncometabolite 2-hydroxyglutarate, supporting the role of mutant IDH-produced 2-hydroxyglutarate as an inhibitor of TET-mediated DNA demethylation. Meta-analysis of the acute myeloid leukaemia, low-grade glioma, cholangiocarcinoma and CS methylation data identifies cancer-specific effectors within the retinoic acid receptor activation pathway among the hypermethylated targets. By analysing sequence motifs surrounding hypermethylated sites across the four cancer types, and using chromatin immunoprecipitation and western blotting, we identify the transcription factor EBF1 (early B-cell factor 1) as an interaction partner for TET2, suggesting a sequence-specific mechanism for regulating DNA methylation.

Indexed as

Bile Duct NeoplasmsBone NeoplasmsCentral Nervous System NeoplasmsCholangiocarcinomaChondrosarcomaDioxygenasesDNA-Binding ProteinsDNA MethylationGene Expression Regulation, NeoplasticGliomaGlutaratesHumansIsocitrate DehydrogenaseLeukemia, Myeloid, AcuteMutationNeoplasmsalpha-hydroxyglutarateDioxygenasesDNA-Binding ProteinsEBF1 protein, humanGlutaratesIDH1 protein, humanIDH2 protein, humanIsocitrate DehydrogenaseProto-Oncogene ProteinsReceptors, Retinoic AcidTET2 protein, humanTrans-Activators

Identifiers

PMID23863747
PMCPMC3759038
OpenAlexW2152807349

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.