Evidence map›Paper›PMID 25990542›Full record

ArticleMolecular oncology2015

Genome methylation patterns in male breast cancer - Identification of an epitype with hypermethylation of polycomb target genes.

Ida Johansson, Martin Lauss, Karolina Holm, Johan Staaf, Cecilia Nilsson, Marie-Louise Fjällskog, Markus Ringnér, Ingrid Hedenfalk

Open access · greenAbstract read
In one paragraph

Article in Molecular oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Male breast cancer: an update.Virchows Archiv : an international journal of pathology · 2022
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
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

8 authors at 2 institutions in 1 country.

Ida JohanssonDepartment of Oncology and Pathology, Clinical Sciences, and CREATE Health Strategic Center for Translational Cancer Research, Lund University, Lund, Sweden.
Martin LaussDepartment of Oncology and Pathology, Clinical Sciences, and CREATE Health Strategic Center for Translational Cancer Research, Lund University, Lund, Sweden.
Karolina HolmDepartment of Oncology and Pathology, Clinical Sciences, and CREATE Health Strategic Center for Translational Cancer Research, Lund University, Lund, Sweden.
Johan StaafDepartment of Oncology and Pathology, Clinical Sciences, and CREATE Health Strategic Center for Translational Cancer Research, Lund University, Lund, Sweden.
Cecilia NilssonDepartment of Oncology, Uppsala University, Uppsala, Sweden.
Marie-Louise FjällskogDepartment of Oncology, Uppsala University, Uppsala, Sweden.
Markus RingnérDepartment of Oncology and Pathology, Clinical Sciences, and CREATE Health Strategic Center for Translational Cancer Research, Lund University, Lund, Sweden.
Ingrid HedenfalkDepartment of Oncology and Pathology, Clinical Sciences, and CREATE Health Strategic Center for Translational Cancer Research, Lund University, Lund, Sweden. Electronic address: Ingrid.Hedenfalk@med.lu.se.
Lund University · SEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Male breast cancer (MBC) is a rare disease that shares both similarities and differences with female breast cancer (FBC). The aim of this study was to assess genome-wide DNA methylation profiles in MBC and compare them with the previously identified transcriptional subgroups of MBC, luminal M1 and M2, as well as the intrinsic subtypes of FBC. Illumina's 450K Infinium arrays were applied to 47 MBC and 188 FBC tumors. Unsupervised clustering of the most variable CpGs among MBC tumors revealed two stable epitypes, designated ME1 and ME2. The methylation patterns differed significantly between the groups and were closely associated with the transcriptional subgroups luminal M1 and M2. Tumors in the ME1 group were more proliferative and aggressive than ME2 tumors, and showed a tendency toward inferior survival. ME1 tumors also displayed hypermethylation of PRC2 target genes and high expression of EZH2, one of the core components of PRC2. Upon combined analysis of MBC and FBC tumors, ME1 MBCs clustered among luminal B FBC tumors and ME2 MBCs clustered within the predominantly luminal A FBC cluster. The majority of the MBC tumors remained grouped together within the clusters rather than being interspersed among the FBC tumors. Differences in the genomic location of methylated CpGs, as well as in the regulation of central canonical pathways may explain the separation between MBC and FBC tumors in the respective clusters. These findings further suggest that MBC is not readily defined using conventional criteria applied to FBC.

Indexed as

DNA MethylationAdultAgedAged, 80 and overBreast Neoplasms, MaleCluster AnalysisGene Expression ProfilingGene Expression Regulation, NeoplasticGenome, HumanGenotypeHumansMaleMiddle AgedPolycomb-Group ProteinsPolycomb-Group ProteinsEpitypeEZH2JARID1BMale breast cancerMethylationPolycomb target genes

Identifiers

PMID25990542
PMCPMC5528783
OpenAlexW2097788588

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.