Evidence map›Paper›PMID 32047165›Full record

ArticleNature communications2020

Androgen receptor-binding sites are highly mutated in prostate cancer.

Tunç Morova, Daniel R McNeill, Nada Lallous, Mehmet Gönen, Kush Dalal, David M Wilson, Attila Gürsoy, Özlem Keskin, Nathan A Lack

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
6.1field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 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

9 authors at 3 institutions in 4 countries.

Tunç MorovaSchool of Medicine, Koç University, Istanbul, 34450, Turkey.
Daniel R McNeillLaboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD, 20892, USA.
Nada LallousVancouver Prostate Centre, University of British Columbia, Vancouver, V6H 3Z6, BC, Canada.
Mehmet GönenSchool of Medicine, Koç University, Istanbul, 34450, Turkey.
Kush DalalVancouver Prostate Centre, University of British Columbia, Vancouver, V6H 3Z6, BC, Canada.
David M WilsonLaboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD, 20892, USA.
Attila GürsoyCollege of Engineering, Koç University, Istanbul, 34450, Turkey.ORCID http://orcid.org/0000-0002-2297-2113
Özlem KeskinCollege of Engineering, Koç University, Istanbul, 34450, Turkey.
Nathan A LackSchool of Medicine, Koç University, Istanbul, 34450, Turkey. nlack@ku.edu.tr.
Koç University · TRNational Institute on Aging · USUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Androgen receptor (AR) signalling is essential in nearly all prostate cancers. Any alterations to AR-mediated transcription can have a profound effect on carcinogenesis and tumor growth. While mutations of the AR protein have been extensively studied, little is known about those somatic mutations that occur at the non-coding regions where AR binds DNA. Using clinical whole genome sequencing, we show that AR binding sites have a dramatically increased rate of mutations that is greater than any other transcription factor and specific to only prostate cancer. Demonstrating this may be common to lineage-specific transcription factors, estrogen receptor binding sites were also found to have elevated rate of mutations in breast cancer. We provide evidence that these mutations at AR binding sites, and likely other related transcription factors, are caused by faulty repair of abasic sites. Overall, this work demonstrates that non-coding AR binding sites are frequently mutated in prostate cancer and can impact enhancer activity.

Indexed as

MutationAnimalsBinding SitesCell Line, TumorDNA-(Apurinic or Apyrimidinic Site) LyaseGene Expression Regulation, NeoplasticMaleMiceMutation RateProstatic NeoplasmsReceptors, AndrogenReceptors, EstrogenTranscription FactorsApex1 protein, mouseAR protein, mouseDNA-(Apurinic or Apyrimidinic Site) LyaseReceptors, AndrogenReceptors, EstrogenTranscription Factors

Identifiers

PMID32047165
PMCPMC7012874
OpenAlexW3006609363

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.