Evidence map›Paper›PMID 32094298›Full record

ReviewCancer research2020

Shaping Chromatin States in Prostate Cancer by Pioneer Transcription Factors.

William Hankey, Zhong Chen, Qianben Wang

Open access · greenAbstract readReview
In one paragraph

Review in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
6.7field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Review
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  8. Crucial roles of mesenchymalProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  10. Circadian regulator REV-ERBα is a master regulator of tumor lineage plasticity and an effective therapeutic target.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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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

3 authors at 1 institution in 1 country.

William HankeyDepartment of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, North Carolina.ORCID 0000-0001-5935-2391
Zhong ChenDepartment of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, North Carolina. qianben.wang@duke.edu zhong.chen128@duke.edu.
Qianben WangDepartment of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, North Carolina. qianben.wang@duke.edu zhong.chen128@duke.edu.ORCID 0000-0003-2636-7145
Duke University · US

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI JOHN N. NORTON · 1985 to 2026
$174.8M
Systems Analysis of Epigenomic Architecture in Cancer ProgressionU54CA217297 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HUANG, TIM H.-M. · 2017 to 2021
$9.3M
Preparing Genetic Counselors for Genomic Medicine ResearchT32HG008955 · NHGRI · DUKE UNIVERSITY · PI COONEY, KATHLEEN A, HAGA, SUSANNE · 2017 to 2021
$2.0M
Role of oncogenic phosphorylated MED1 in aggressive prostate cancerR01CA200853 · NCI · OHIO STATE UNIVERSITY · PI CLINTON, STEVEN K, HUANG, JIAOTI · 2017 to 2021
$1.9M
Novel genomic mechanism for ligand-dependent transcription by androgen receptorR01GM120221 · NIGMS · OHIO STATE UNIVERSITY · PI WANG, QIANBEN · 2017 to 2020
$1.3M
NCI NIH HHS P30 CA014236NCI NIH HHS R01 CA200853NCI NIH HHS U54 CA217297NHGRI NIH HHS T32 HG008955NIGMS NIH HHS R01 GM120221
6 · The paper itself

Abstract

The androgen receptor (AR) is a critical therapeutic target in prostate cancer that responds to antagonists in primary disease, but inevitably becomes reactivated, signaling onset of the lethal castration-resistant prostate cancer (CRPC) stage. Epigenomic investigation of the chromatin environment and interacting partners required for AR transcriptional activity has uncovered three pioneer factors that open up chromatin and facilitate AR-driven transcriptional programs. FOXA1, HOXB13, and GATA2 are required for normal AR transcription in prostate epithelial development and for oncogenic AR transcription during prostate carcinogenesis. AR signaling is dependent upon these three pioneer factors both before and after the clinical transition from treatable androgen-dependent disease to untreatable CRPC. Agents targeting their respective DNA binding or downstream chromatin-remodeling events have shown promise in preclinical studies of CRPC. AR-independent functions of FOXA1, HOXB13, and GATA2 are emerging as well. While all three pioneer factors exert effects that promote carcinogenesis, some of their functions may inhibit certain stages of prostate cancer progression. In all, these pioneer factors represent some of the most promising potential therapeutic targets to emerge thus far from the study of the prostate cancer epigenome.

Indexed as

Antineoplastic AgentsCarcinogenesisChromatinChromatin Assembly and DisassemblyDisease ProgressionEpigenesis, GeneticGATA2 Transcription FactorGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 3-alphaHomeodomain ProteinsHumansMaleProstateProstatic Neoplasms, Castration-ResistantReceptors, AndrogenSignal TransductionAntineoplastic AgentsAR protein, humanChromatinFOXA1 protein, humanGATA2 protein, humanGATA2 Transcription FactorHepatocyte Nuclear Factor 3-alphaHomeodomain ProteinsHOXB13 protein, humanReceptors, Androgen

Identifiers

PMID32094298
PMCPMC7299826
OpenAlexW3008752748

What OpenQuestion holds

Textmetadata
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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.