Evidence map›Paper›PMID 26880803›Full record

ArticleCancer research2016

Deletion of Interstitial Genes between TMPRSS2 and ERG Promotes Prostate Cancer Progression.

Douglas E Linn, Kathryn L Penney, Roderick T Bronson, Lorelei A Mucci, Zhe Li

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Evolution of AR and Non-AR Alterations in ctDNA of Patients with Metastatic Prostate Cancer Treated in the Phase III Alliance A031201 Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Trial
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  5. Proceedings of the National Academy of Sciences of the United States of America · 2024
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  11. Cancers · 2021
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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

5 authors at 1 institution in 1 country.

Douglas E LinnDivision of Genetics, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, Boston, Massachusetts.
Kathryn L PenneyChanning Division of Network Medicine, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, Boston, Massachusetts. Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts.
Roderick T BronsonRodent Histopathology, Harvard Medical School, Boston, Massachusetts.
Lorelei A MucciChanning Division of Network Medicine, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, Boston, Massachusetts. Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts.
Zhe LiDivision of Genetics, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, Boston, Massachusetts. zli4@rics.bwh.harvard.edu.
Harvard University · US

Funding

Tumor and Circulating Markers as Links Between Obesity and Lethal Prostate CanceP50CA090381 · NCI · DANA-FARBER CANCER INSTITUTE · PI LODA, MASSIMO · 2002 to 2017
$36.2M
Sex-Hormones and the TMPRSS2: ERG Fusion in Prostate Cancer ProgressionR01CA136578 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI MUCCI, LORELEI · 2009 to 2013
$1.7M
NCI NIH HHS P50 CA090381NCI NIH HHS R01 CA136578
6 · The paper itself

Abstract

TMPRSS2-ERG gene fusions that occur frequently in human prostate cancers can be generated either through insertional chromosomal rearrangement or by intrachromosomal deletion. Genetically, a key difference between these two mechanisms is that the latter results in deletion of a ∼3-Mb interstitial region containing genes with unexplored roles in prostate cancer. In this study, we characterized two mouse models recapitulating TMPRSS2-ERG insertion or deletion events in the background of prostate-specific PTEN deficiency. We found that only the mice that lacked the interstitial region developed prostate adenocarcinomas marked by poor differentiation and epithelial-to-mesenchymal transition. Mechanistic investigations identified several interstitial genes, including Ets2 and Bace2, whose reduced expression correlated in the gene homologs in human prostate cancer with biochemical relapse and lethal disease. Accordingly, PTEN-deficient mice with prostate-specific knockout of Ets2 exhibited marked progression of prostate adenocarcinomas that was partly attributed to activation of MAPK signaling. Collectively, our findings established that Ets2 is a tumor suppressor gene in prostate cancer, and its loss along with other genes within the TMPRSS2-ERG interstitial region contributes to disease progression. Cancer Res; 76(7); 1869-81. ©2016 AACR.

Indexed as

AnimalsDisease ProgressionElectroretinographyGene Expression ProfilingHumansMaleMiceProstatic NeoplasmsSerine EndopeptidasesSerine EndopeptidasesTMPRSS2 protein, human

Identifiers

PMID26880803
PMCPMC4873435
OpenAlexW2285177102

What OpenQuestion holds

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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.