Evidence map›Paper›PMID 19156837›Full record

ArticleGenes, chromosomes & cancer2009

Distinct genomic aberrations associated with ERG rearranged prostate cancer.

Francesca Demichelis, Sunita R Setlur, Rameen Beroukhim, Sven Perner, Jan O Korbel, Christopher J Lafargue, Dorothee Pflueger, Cara Pina, Matthias D Hofer, Andrea Sboner and 9 more

Open access · greenAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
6.2field-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

55 citing papers in PubMed, 89 citations in OpenAlex.

  1. Trial
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  3. Review
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  5. Review
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  7. Article
  8. Review
  9. Triple Aberrant Prostate Cancer (TAPC) - Aggregate role of aberrations inAmerican journal of clinical and experimental urology · 2020
    Article
  10. Article
  11. The Genomics of Prostate Cancer: A Historic Perspective.Cold Spring Harbor perspectives in medicine · 2019
    Review
  12. Molecular Composition of GenomicDisease markers · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. 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

19 authors at 6 institutions in 2 countries.

Francesca DemichelisDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical Center, New York, NY 10065.
Sunita R Setlur
Rameen Beroukhim
Sven Perner
Jan O Korbel
Christopher J Lafargue
Dorothee Pflueger
Cara Pina
Matthias D Hofer
Andrea Sboner
Maria A Svensson
David S Rickman
Alex Urban
Michael Snyder
Matthew Meyerson
Charles Lee
Mark B Gerstein
Rainer Kuefer
Mark A Rubin
Cornell University · USYale University · USBrigham and Women's Hospital · USBroad Institute · USUniversity Hospital Ulm · DEHarvard University · US

Funding

Molecular Signatures of Lethal and Indolent Prostate CancerR01CA116337 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI RUBIN, MARK A. · 2006 to 2016
$5.3M
NKX2-1, A Candidate Lineage Survival Oncogene in Lung AdenocarcinomaR01CA109038 · NCI · DANA-FARBER CANCER INSTITUTE · PI MEYERSON, MATTHEW L. · 2005 to 2014
$3.8M
Towards Understanding Prostate Cancer HeterogeneityR01CA125612 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI RUBIN, MARK A. · 2007 to 2017
$3.4M
High-resolution genome-wide mapping of structural mutations in prostate cancerK08CA122833 · NCI · DANA-FARBER CANCER INST · PI BEROUKHIM, RAMEEN · 2007 to 2011
$697k
NCI NIH HHS 5K08CA122833-02NCI NIH HHS K08 CA122833NCI NIH HHS R01 CA109038NCI NIH HHS R01CA109038NCI NIH HHS R01 CA116337NCI NIH HHS R01CA116337NCI NIH HHS R01 CA125612NCI NIH HHS R01CA125612PHS HHS PCO40715
6 · The paper itself

Abstract

Emerging molecular and clinical data suggest that ETS fusion prostate cancer represents a distinct molecular subclass, driven most commonly by a hormonally regulated promoter and characterized by an aggressive natural history. The study of the genomic landscape of prostate cancer in the light of ETS fusion events is required to understand the foundation of this molecularly and clinically distinct subtype. We performed genome-wide profiling of 49 primary prostate cancers and identified 20 recurrent chromosomal copy number aberrations, mainly occurring as genomic losses. Co-occurring events included losses at 19q13.32 and 1p22.1. We discovered three genomic events associated with ERG rearranged prostate cancer, affecting 6q, 7q, and 16q. 6q loss in nonrearranged prostate cancer is accompanied by gene expression deregulation in an independent dataset and by protein deregulation of MYO6. To analyze copy number alterations within the ETS genes, we performed a comprehensive analysis of all 27 ETS genes and of the 3 Mbp genomic area between ERG and TMPRSS2 (21q) with an unprecedented resolution (30 bp). We demonstrate that high-resolution tiling arrays can be used to pin-point breakpoints leading to fusion events. This study provides further support to define a distinct molecular subtype of prostate cancer based on the presence of ETS gene rearrangements.

Indexed as

Chromosome AberrationsGene RearrangementCell Line, TumorChromosome MappingGene Expression Regulation, NeoplasticHumansIn Situ Hybridization, FluorescenceMaleOligonucleotide Array Sequence AnalysisProstatic NeoplasmsProto-Oncogene Proteins c-etsTrans-ActivatorsTranscriptional Regulator ERGERG protein, humanProto-Oncogene Proteins c-etsTrans-ActivatorsTranscriptional Regulator ERG

Identifiers

PMID19156837
PMCPMC2674964
OpenAlexW2105460321

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.