Evidence map›Paper›PMID 27851974›Full record

ArticleCell reports2016

eFORGE: A Tool for Identifying Cell Type-Specific Signal in Epigenomic Data.

Charles E Breeze, Dirk S Paul, Jenny van Dongen, Lee M Butcher, John C Ambrose, James E Barrett, Robert Lowe, Vardhman K Rakyan, Valentina Iotchkova, Mattia Frontini and 17 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 11 pooled it
–field-weighted citation impact
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

91 citing papers in PubMed, 11 syntheses or guidelines pooled it.

  1. Pooled it
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  8. Epigenome-wide meta-analysis of DNA methylation and childhood asthma.The Journal of allergy and clinical immunology · 2019
    Pooled it
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  18. Smoking drives an epigenetic memory of aberrant hematopoiesis.medRxiv : the preprint server for health sciences · 2026
    Article
  19. Article
  20. Article

31 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

27 authors.

Charles E BreezeUCL Cancer Institute, University College London, London WC1E 6BT, UK. Electronic address: c.breeze@ucl.ac.uk.
Dirk S PaulUCL Cancer Institute, University College London, London WC1E 6BT, UK.
Jenny van DongenDepartment of Biological Psychology, Vrije Universiteit Amsterdam, 1081BT Amsterdam, the Netherlands.
Lee M ButcherUCL Cancer Institute, University College London, London WC1E 6BT, UK; Department of Surgery and Cancer, Imperial College London, London W12 0NN, UK.
John C AmbroseUCL Cancer Institute, University College London, London WC1E 6BT, UK.
James E BarrettUCL Cancer Institute, University College London, London WC1E 6BT, UK.
Robert LoweBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, E1 2AT London, UK.
Vardhman K RakyanBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, E1 2AT London, UK.
Valentina IotchkovaEuropean Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI), Wellcome Genome Campus, Hinxton, Cambridge CB10 1SD, UK; Department of Human Genetics, The Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge CB10 1HH, UK.
Mattia FrontiniDepartment of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge CB2 0PT, UK; National Health Service (NHS) Blood and Transplant, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge CB2 0PT, UK; British Heart Foundation Centre of Excellence, Cambridge Biomedical Campus, Long Road, Cambridge CB2 0QQ, UK.
Kate DownesDepartment of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge CB2 0PT, UK; National Health Service (NHS) Blood and Transplant, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge CB2 0PT, UK.
Willem H OuwehandDepartment of Human Genetics, The Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge CB10 1HH, UK; Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge CB2 0PT, UK; National Health Service (NHS) Blood and Transplant, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge CB2 0PT, UK; British Heart Foundation Centre of Excellence, Cambridge Biomedical Campus, Long Road, Cambridge CB2 0QQ, UK.
Jonathan LaperleDépartement d'Informatique, Université de Sherbrooke, Sherbrooke, QC J1K 2R1, Canada.
Pierre-Étienne JacquesDépartement d'Informatique, Université de Sherbrooke, Sherbrooke, QC J1K 2R1, Canada; Département de Biologie, Université de Sherbrooke, Sherbrooke, QC J1K 2R1, Canada; Centre de recherche du Centre hospitalier universitaire de Sherbrooke, Sherbrooke, QC J1H 5N4, Canada.
Guillaume BourqueDepartment of Human Genetics, McGill University, Montréal, QC H3G 1Y6, Canada; Génome Québec Innovation Center, Montréal, QC H3A 0G1, Canada.
Anke K BergmannInstitute of Human Genetics, Christian Albrechts University, 24105 Kiel, Germany; Department of Pediatrics, Christian-Albrechts-University Kiel & University Hospital Schleswig-Holstein, 24105 Kiel, Germany.
Reiner SiebertInstitute of Human Genetics, Christian Albrechts University, 24105 Kiel, Germany; Institute of Human Genetics, University of Ulm, Albert-Einstein-Allee 11, 89081 Ulm, Germany.
Edo VellengaDepartment of Hematology, University of Groningen and University Medical Center Groningen, PO Box 30001, 9700 RB Groningen, the Netherlands.
Sadia SaeedDepartment of Biochemistry, PMAS Arid Agriculture University Rawalpindi, 46300 Rawalpindi, Pakistan; Department of Molecular Biology, Faculty of Science, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, the Netherlands.
Filomena MatareseDepartment of Molecular Biology, Faculty of Science, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, the Netherlands.
Joost H A MartensDepartment of Molecular Biology, Faculty of Science, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, the Netherlands.
Hendrik G StunnenbergDepartment of Molecular Biology, Faculty of Science, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, the Netherlands.
Andrew E TeschendorffUCL Cancer Institute, University College London, London WC1E 6BT, UK.
Javier HerreroUCL Cancer Institute, University College London, London WC1E 6BT, UK.
Ewan BirneyEuropean Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI), Wellcome Genome Campus, Hinxton, Cambridge CB10 1SD, UK.
Ian DunhamEuropean Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI), Wellcome Genome Campus, Hinxton, Cambridge CB10 1SD, UK.
Stephan BeckUCL Cancer Institute, University College London, London WC1E 6BT, UK. Electronic address: s.beck@ucl.ac.uk.

Funding

British Heart Foundation RG/09/012/28096Department of Health RP-PG-0310-1002Medical Research Council G0800270Wellcome Trust 99148
6 · The paper itself

Abstract

Epigenome-wide association studies (EWAS) provide an alternative approach for studying human disease through consideration of non-genetic variants such as altered DNA methylation. To advance the complex interpretation of EWAS, we developed eFORGE (http://eforge.cs.ucl.ac.uk/), a new standalone and web-based tool for the analysis and interpretation of EWAS data. eFORGE determines the cell type-specific regulatory component of a set of EWAS-identified differentially methylated positions. This is achieved by detecting enrichment of overlap with DNase I hypersensitive sites across 454 samples (tissues, primary cell types, and cell lines) from the ENCODE, Roadmap Epigenomics, and BLUEPRINT projects. Application of eFORGE to 20 publicly available EWAS datasets identified disease-relevant cell types for several common diseases, a stem cell-like signature in cancer, and demonstrated the ability to detect cell-composition effects for EWAS performed on heterogeneous tissues. Our approach bridges the gap between large-scale epigenomics data and EWAS-derived target selection to yield insight into disease etiology.

Indexed as

EpigenomicsSignal TransductionSoftwareStatistics as TopicDNA MethylationGenome-Wide Association StudyHumansKaryotypingMultiple SclerosisOrgan SpecificityStem CellsbioinformaticsDNase I hypersensitive sitesepigeneticsepigenome-wide association studyhistone marks

Identifiers

PMID27851974
PMCPMC5120369

What OpenQuestion holds

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Registered trials

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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.