Evidence map›Paper›PMID 37902007›Full record

ArticleEMBO molecular medicine2023

Luminal breast cancer identity is determined by loss of glucocorticoid receptor activity.

Stefan Prekovic, Theofilos Chalkiadakis, Merel Roest, Daniel Roden, Catrin Lutz, Karianne Schuurman, Mark Opdam, Liesbeth Hoekman, Nina Abbott, Tanja Tesselaar and 15 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2023. 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
7.8field-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

14 citing papers in PubMed, 25 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors at 7 institutions in 4 countries.

Stefan Prekovic *Division of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0002-7051-9321
Theofilos Chalkiadakis *Center for Molecular Medicine, UMC Utrecht, Utrecht, The Netherlands.
Merel Roest *Division of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Daniel RodenCancer Ecosystems Program, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
Catrin LutzDivision of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Karianne SchuurmanDivision of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0002-9278-0571
Mark OpdamDivision of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0001-5832-6386
Liesbeth HoekmanMass Spectrometry/Proteomics Facility, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0002-3552-6390
Nina AbbottDivision of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Tanja TesselaarDivision of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Maliha WajahatDame Roma Mitchell Cancer Research Laboratories, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.
Amy R DwyerDame Roma Mitchell Cancer Research Laboratories, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.
Isabel Mayayo-PeraltaDivision of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Gabriela GomezSchool of Pharmacy and Biomolecular Sciences, The Royal College of Surgeons University of Medicine and Health Sciences, Dublin, Ireland.ORCID 0000-0002-4367-4414
Maarten AltelaarMass Spectrometry/Proteomics Facility, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0001-5093-5945
Roderick BeijersbergenDivision of Molecular Carcinogenesis and Robotics and Screening Centre, Netherlands Cancer Institute, Amsterdam, The Netherlands.
Balázs GyőrffyTTK Cancer Biomarker Research Group, Institute of Enzymology, Budapest, Hungary.ORCID 0000-0002-5772-3766
Leonie YoungEndocrine Oncology Research Group, Department of Surgery, The Royal College of Surgeons University of Medicine and Health Sciences, Dublin, Ireland.
Sabine LinnDivision of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Jos JonkersDivision of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0002-9264-9792
Wayne TilleyDame Roma Mitchell Cancer Research Laboratories, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.ORCID 0000-0003-1893-2626
Theresa HickeyDame Roma Mitchell Cancer Research Laboratories, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.ORCID 0000-0002-2752-730X
Damir VareslijaSchool of Pharmacy and Biomolecular Sciences, The Royal College of Surgeons University of Medicine and Health Sciences, Dublin, Ireland.ORCID 0000-0003-1000-0357
Alexander SwarbrickCancer Ecosystems Program, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.ORCID 0000-0002-3051-5676
Wilbert ZwartDivision of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0002-9823-7289
The Netherlands Cancer Institute · NLRoyal College of Surgeons in Ireland · IEThe University of Adelaide · AUUtrecht University · NLNew South Wales Department of Health · AUFreemasons Foundation Centre for Men's Health · AUSemmelweis University · HU

Funding

KWF Kankerbestrijding (DCS) 12128Nederlandse Organisatie voor Wetenschappelijk Onderzoek (NWO) 91716401Oncode Institute
6 · The paper itself

Abstract

Glucocorticoid receptor (GR) is a transcription factor that plays a crucial role in cancer biology. In this study, we utilized an in silico-designed GR activity signature to demonstrate that GR relates to the proliferative capacity of numerous primary cancer types. In breast cancer, the GR activity status determines luminal subtype identity and has implications for patient outcomes. We reveal that GR engages with estrogen receptor (ER), leading to redistribution of ER on the chromatin. Notably, GR activation leads to upregulation of the ZBTB16 gene, encoding for a transcriptional repressor, which controls growth in ER-positive breast cancer and associates with prognosis in luminal A patients. In relation to ZBTB16's repressive nature, GR activation leads to epigenetic remodeling and loss of histone acetylation at sites proximal to cancer-driving genes. Based on these findings, epigenetic inhibitors reduce viability of ER-positive breast cancer cells that display absence of GR activity. Our findings provide insights into how GR controls ER-positive breast cancer growth and may have implications for patients' prognostication and provide novel therapeutic candidates for breast cancer treatment.

Indexed as

Breast NeoplasmsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansReceptors, EstrogenReceptors, GlucocorticoidReceptors, EstrogenReceptors, Glucocorticoidbreast cancerglucocorticoidsluminal breast cancer subtypesnuclear receptorsZBTB16

Identifiers

PMID37902007
PMCPMC10701603
OpenAlexW4388014565

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.