Evidence map›Paper›PMID 36725920›Full record

ArticleBritish journal of cancer2023

Chromatin profile-based identification of a novel ER-positive breast cancer subgroup with reduced ER-responsive element accessibility.

Kohei Kumegawa, Sumito Saeki, Yoko Takahashi, Liying Yang, Tomo Osako, Tomoyoshi Nakadai, Sayuri Amino, Tetsuyo Maeda, Chikako Takahata, Seiichi Mori and 4 more

Erratum issuedOpen access · hybridFull text read
In one paragraph

Article in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

3 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 1 institution in 1 country.

Kohei Kumegawa *Cancer Cell Diversity Project, NEXT-Ganken Program, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID 0000-0003-3732-2874
Sumito Saeki *Breast Surgical Oncology, Breast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Yoko Takahashi *Breast Surgical Oncology, Breast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Liying YangProject for Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Tomo OsakoDivision of Pathology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID 0000-0001-9250-4035
Tomoyoshi NakadaiProject for Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Sayuri AminoProject for Development of Innovative Research on Cancer Therapeutics, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Tetsuyo MaedaBreast Surgical Oncology, Breast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Chikako TakahataBreast Surgical Oncology, Breast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Seiichi MoriProject for Development of Innovative Research on Cancer Therapeutics, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Tetsuo NodaDirector's room, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Shinji OhnoBreast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Takayuki UenoBreast Surgical Oncology, Breast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID 0000-0002-9080-9377
Reo MaruyamaCancer Cell Diversity Project, NEXT-Ganken Program, Japanese Foundation for Cancer Research, Tokyo, Japan. reo.maruyama@jfcr.or.jp.ORCID 0000-0001-7166-5964
Japanese Foundation For Cancer Research · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOestrogen receptor (ER) signalling-dependent cancer cell growth is one of the major features of ER-positive breast cancer (BC). Inhibition of ER function is a standard and effective treatment for ER-positive tumours; however, ~20% of patients with ER-positive BC experience early or late recurrence. In this study, we examined intertumour heterogeneity from an epigenetic perspective based on the hypothesis that the intrinsic difference in epigenetic states around ER signalling pathway underlies endocrine therapy resistance.

methodsWe performed transposase-accessible chromatin sequencing (ATAC-seq) analysis of 42 BC samples, including 35 ER-positive(+) human epidermal growth factor receptor 2 (HER2)-negative(-) and 7 triple-negative tumours. We also reanalysed ATAC-seq data of 45 ER + /HER2 - tumours in the Cancer Genome Atlas (TCGA) BC cohort to validate our observations.

resultsWe conducted a comprehensive analysis of cis-regulatory elements (CREs) using ATAC-seq, identifying three subgroups based on chromatin accessibility profiles. We identified a subgroup of ER-positive BCs with a distinctive chromatin accessibility pattern including reduced accessibility to ER-responsive elements (EREs). The same subgroup was also observed in TCGA BC cohort. Despite the reduced accessibility to EREs, the expression of ER and potential ER target genes were not decreased in these tumours.

conclusionOur findings highlight the existence of a subset of ER-positive BCs with unchanged ER expression but reduced EREs accessibility that cannot be distinguished by conventional immunostaining for ER. Future studies should determine whether these tumours are associated with resistance to endocrine therapy.

Indexed as

Breast NeoplasmsChromatinFemaleHumansReceptors, EstrogenSignal TransductionTreatment OutcomeChromatinReceptors, Estrogen

Identifiers

PMID36725920
PMCPMC10050410
OpenAlexW4318775821

What OpenQuestion holds

Textfull text, public
LicenceCC BY
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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.