Evidence map›Paper›PMID 29099283›Full record

ArticleEpigenetics2017

Lowly methylated region analysis identifies EBF1 as a potential epigenetic modifier in breast cancer.

Nora Fernandez-Jimenez, Athena Sklias, Szilvia Ecsedi, Vincent Cahais, Davide Degli-Esposti, Antonin Jay, Pierre Benoit Ancey, Hae Dong Woo, Hector Hernandez-Vargas, Zdenko Herceg

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Nora Fernandez-Jimeneza Epigenetics Group , International Agency for Research on Cancer (IARC) , Lyon Cedex 08, France.
Athena Skliasa Epigenetics Group , International Agency for Research on Cancer (IARC) , Lyon Cedex 08, France.
Szilvia Ecsedia Epigenetics Group , International Agency for Research on Cancer (IARC) , Lyon Cedex 08, France.
Vincent Cahaisa Epigenetics Group , International Agency for Research on Cancer (IARC) , Lyon Cedex 08, France.
Davide Degli-Espostia Epigenetics Group , International Agency for Research on Cancer (IARC) , Lyon Cedex 08, France.
Antonin Jaya Epigenetics Group , International Agency for Research on Cancer (IARC) , Lyon Cedex 08, France.
Pierre Benoit Anceya Epigenetics Group , International Agency for Research on Cancer (IARC) , Lyon Cedex 08, France.
Hae Dong Wooa Epigenetics Group , International Agency for Research on Cancer (IARC) , Lyon Cedex 08, France.
Hector Hernandez-Vargasa Epigenetics Group , International Agency for Research on Cancer (IARC) , Lyon Cedex 08, France.
Zdenko Hercega Epigenetics Group , International Agency for Research on Cancer (IARC) , Lyon Cedex 08, France.
Centre International de Recherche sur le Cancer · FR

Funding

World Health Organization 001
6 · The paper itself

Abstract

Breast cancer (BC) encompasses heterogeneous pathologies with different subtypes exhibiting distinct molecular changes, including those related to DNA methylation. However, the role of these changes in mediating BC heterogeneity is poorly understood. Lowly methylated regions (LMRs), non-CpG island loci that usually contain transcription factor (TF) binding sites, have been suggested to act as regulatory elements that define cellular identity. In this study, we aimed to identify the key subtype-specific TFs that may lead to LMR generation and shape the BC methylome and transcription program. We initially used whole-genome bisulfite sequencing (WGBS) data available at The Cancer Genome Atlas (TCGA) portal to identify subtype-specific LMRs. Differentially methylated regions (DMRs) within the BC PAM50 subtype-specific LMRs were selected by comparing tumors and normal tissues in a larger TCGA cohort assessed by HumanMethylation450 BeadChip (450K) arrays and TF enrichment analyses were performed. To assess the impact of LMRs on gene expression, TCGA RNA sequencing data were downloaded and Pearson correlations between methylation levels of loci presenting subtype-specific TF motifs and expression of the nearest genes were calculated. WGBS methylome data revealed a large number of LMRs for each of the BC subtypes. Analysis of these LMRs in the 450K datasets available for a larger sample set identified 7,765, 5,657, and 19 differentially methylated positions (DMPs) between normal adjacent tissues and tumor tissues from basal, luminal, and HER2-enriched subtypes, respectively. Unsupervised clustering showed that the discriminatory power of the top DMPs was remarkably strong for basal BC. Interestingly, in this particular subtype, we found 4,409 differentially hypomethylated positions grouped into 1,185 DMRs with a strong enrichment for the early B-cell factor 1 (EBF1) motifs. The methylation levels of the DMRs containing EBF1 motifs showed a strong negative correlation with the expression of 719 nearby genes, including BTS2 and CD74, two oncogenes known to be specific for basal BC subtype and for poor outcome. This study identifies LMRs specific to the three main BC subtypes and reveals EBF1 as a potentially important regulator of BC subtype-specific methylation and gene expression program.

Indexed as

DNA MethylationEpigenesis, GeneticGenes, ModifierBreast NeoplasmsFemaleGene Expression Regulation, NeoplasticHumansTrans-ActivatorsEBF1 protein, humanTrans-Activatorsbreast cancer subtypesDNA methylomeEBF1lowly methylated regionstranscription factor binding sites

Identifiers

PMID29099283
PMCPMC5788421
OpenAlexW2765569049

What OpenQuestion holds

Textmetadata
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.