Evidence map›Paper›PMID 29761525›Full record

ArticleThe Prostate2018

ETS2 is a prostate basal cell marker and is highly expressed in prostate cancers aberrantly expressing p63.

Alba Torres, Mohammed Alshalalfa, Elai Davicioni, Anuj Gupta, Srinivasan Yegnasubramanian, Sarah J Wheelan, Jonathan I Epstein, Angelo M De Marzo, Tamara L Lotan

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2018. 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
1.6field-weighted citation impact, top 16% 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.

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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 2 institutions in 2 countries.

Alba TorresDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, Maryland.
Mohammed AlshalalfaGenomeDx Biosciences, Vancouver, British Columbia.
Elai DavicioniGenomeDx Biosciences, Vancouver, British Columbia.
Anuj GuptaDepartment of Oncology, Johns Hopkins School of Medicine, Baltimore, Maryland.
Srinivasan YegnasubramanianDepartment of Oncology, Johns Hopkins School of Medicine, Baltimore, Maryland.
Sarah J WheelanDepartment of Oncology, Johns Hopkins School of Medicine, Baltimore, Maryland.
Jonathan I EpsteinDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, Maryland.ORCID 0000-0003-1839-6472
Angelo M De MarzoDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, Maryland.
Tamara L LotanDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, Maryland.ORCID 0000-0002-0494-9067
Johns Hopkins University · USGenome British Columbia · CA

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI WILLIAM George NELSON · 1985 to 2026
$208.6M
TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
Multidiciplinary Integrative Genomic Approach to Distinguish Lethal from Indolent Prostate Cancer in Men of Europena and African AncestryU01CA196390 · NCI · JOHNS HOPKINS UNIVERSITY · PI DE MARZO, ANGELO MICHAEL, PIENTA, KENNETH J. · 2015 to 2020
$5.8M
NCI NIH HHS P50 CA058236NCI NIH HHS U01 CA196390
6 · The paper itself

Abstract

backgroundRare prostate carcinomas aberrantly express p63 and have an immunophenotype intermediate between basal and luminal cells. Here, we performed gene expression profiling on p63-expressing prostatic carcinomas and compared them to usual-type adenocarcinoma. We identify ETS2 as highly expressed in p63-expressing prostatic carcinomas and benign prostate basal cells, with lower expression in luminal cells and primary usual-type adenocarcinomas.

methodsA total of 8 p63-expressing prostate carcinomas at radical prostatectomy were compared to 358 usual-type adenocarcinomas by gene expression profiling performed on formalin fixed paraffin embedded tumor tissue using Affymetrix 1.0 ST microarrays. Correlation between differentially expressed genes and TP63 expression was performed in 5239 prostate adenocarcinomas available in the Decipher GRID. For validation, ETS2 in situ hybridization was performed on 19 p63-expressing prostate carcinomas and 30 usual-type adenocarcinomas arrayed on tissue microarrays (TMA).

resultsBy gene expression, p63-expressing prostate carcinomas showed low cell cycle activity and low Decipher prognostic scores, but were predicted to have high Gleason grade compared to usual-type adenocarcinomas by gene expression signatures and morphology. Among the genes over-expressed in p63-expressing carcinoma relative to usual-type adenocarcinoma were known p63-regulated genes, along with ETS2, an ETS family member previously implicated as a prostate cancer tumor suppressor gene. Across several cohorts of prostate samples, ETS2 gene expression was correlated with TP63 expression and was significantly higher in benign prostate compared to usual-type adenocarcinoma. By in situ hybridization, ETS2 gene expression was high in benign basal cells, and low to undetectable in benign luminal cells or usual-type adenocarcinoma. In contrast, ETS2 was highly expressed in 95% (18/19) of p63-expressing prostate carcinomas.

conclusionsETS2 is a predominantly basally-expressed gene in the prostate, with low expression in usual-type adenocarcinoma and high expression in p63-expressing carcinomas. Given this pattern, the significance of ETS2 loss by deletion or mutation in usual-type adenocarcinomas is uncertain.

Indexed as

AdenocarcinomaBiomarkers, TumorGene ExpressionGene Expression ProfilingHumansImmunohistochemistryIn Situ HybridizationMaleProstateProstatectomyProstatic NeoplasmsProto-Oncogene Protein c-ets-2RNATissue Array AnalysisTranscription FactorsTumor Suppressor ProteinsBiomarkers, TumorETS2 protein, humanProto-Oncogene Protein c-ets-2RNATP63 protein, humanTranscription FactorsTumor Suppressor ProteinsETS2gene expressionin situ hybridizationp63prostate basal cellsprostatic carcinoma

Identifiers

PMID29761525
PMCPMC6818503
OpenAlexW2803206837

What OpenQuestion holds

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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.