Evidence map›Paper›PMID 27669432›Full record

ArticleOncogene2017

Cell cycle-coupled expansion of AR activity promotes cancer progression.

C McNair, A Urbanucci, C E S Comstock, M A Augello, J F Goodwin, R Launchbury, S G Zhao, M J Schiewer, A Ertel, J Karnes and 8 more

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  8. Targeting lipid metabolism in metastatic prostate cancer.Therapeutic advances in medical oncology · 2023
    Review
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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

18 authors at 8 institutions in 3 countries.

C McNairDepartment of Cancer Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
A UrbanucciProstate Cancer Research Group, Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo and Oslo University Hospitals, Oslo, Norway.
C E S ComstockDepartment of Cancer Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
M A AugelloDepartment of Cancer Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
J F GoodwinDepartment of Cancer Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
R LaunchburyCambridge Research Institute, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
S G ZhaoDepartment of Radiation Oncology, University of Michigan, Ann Arbor, MI, USA.
M J SchiewerDepartment of Cancer Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
A ErtelDepartment of Cancer Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
J KarnesDivision of Biomedical Statistics and Informatics, Mayo Clinic College of Medicine, Rochester, MN, USA.
E DavicioniGenomeDx Biosciences, San Diego, CA, USA.
L WangDivision of Biomedical Statistics and Informatics, Mayo Clinic College of Medicine, Rochester, MN, USA.
Q WangOhio State University College of Medicine, Columbus, OH, USA.
I G MillsProstate Cancer Research Group, Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo and Oslo University Hospitals, Oslo, Norway.
F Y FengDepartment of Radiation Oncology, Urology, and Medicine and Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, CA, USA.
W LiDan L. Duncan Cancer Center and Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.ORCID 0000-0001-9931-5990
J S CarrollCambridge Research Institute, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
K E KnudsenDepartment of Cancer Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
Thomas Jefferson University · USMayo Clinic · USUniversity of Cambridge · GBOslo University Hospital · NOQueen's University Belfast · GBThe Ohio State University · USUCSF Helen Diller Family Comprehensive Cancer Center · USUniversity of Michigan · US

Funding

X-Ray Crystallography and Macromolecular CharacterizationP30CA056036 · NCI · THOMAS JEFFERSON UNIVERSITY · PI Andrew Chapman · 1995 to 2026
$94.8M
Computational and Experimental Modeling of Alternative PolyadenylationR01CA193466 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI LI, WEI · 2016 to 2025
$3.3M
RB Function in Prostate Cancer ProgressionR01CA176401 · NCI · THOMAS JEFFERSON UNIVERSITY · PI KNUDSEN, KAREN E · 2014 to 2018
$2.2M
Computational and Experimental Modeling of Epigenetic DNA MethylationR01HG007538 · NHGRI · UNIVERSITY OF CALIFORNIA-IRVINE · PI LI, WEI · 2014 to 2018
$1.9M
SWI/SNF dysregulation in development and diseaseR01CA159945 · NCI · THOMAS JEFFERSON UNIVERSITY · PI KNUDSEN, KAREN E · 2012 to 2016
$1.6M
Cancer Research UK 20411NCI NIH HHS P30 CA056036NCI NIH HHS R01 CA159945NCI NIH HHS R01 CA176401NCI NIH HHS R01 CA193466NHGRI NIH HHS R01 HG007538
6 · The paper itself

Abstract

The androgen receptor (AR) is required for prostate cancer (PCa) survival and progression, and ablation of AR activity is the first line of therapeutic intervention for disseminated disease. While initially effective, recurrent tumors ultimately arise for which there is no durable cure. Despite the dependence of PCa on AR activity throughout the course of disease, delineation of the AR-dependent transcriptional network that governs disease progression remains elusive, and the function of AR in mitotically active cells is not well understood. Analyzing AR activity as a function of cell cycle revealed an unexpected and highly expanded repertoire of AR-regulated gene networks in actively cycling cells. New AR functions segregated into two major clusters: those that are specific to cycling cells and retained throughout the mitotic cell cycle ('Cell Cycle Common'), versus those that were specifically enriched in a subset of cell cycle phases ('Phase Restricted'). Further analyses identified previously unrecognized AR functions in major pathways associated with clinical PCa progression. Illustrating the impact of these unmasked AR-driven pathways, dihydroceramide desaturase 1 was identified as an AR-regulated gene in mitotically active cells that promoted pro-metastatic phenotypes, and in advanced PCa proved to be highly associated with development of metastases, recurrence after therapeutic intervention and reduced overall survival. Taken together, these findings delineate AR function in mitotically active tumor cells, thus providing critical insight into the molecular basis by which AR promotes development of lethal PCa and nominate new avenues for therapeutic intervention.

Indexed as

Cell CycleAndrogensBase SequenceBinding SitesCluster AnalysisComputational BiologyDisease ProgressionGene Expression ProfilingGene Expression Regulation, NeoplasticHumansModels, BiologicalNeoplasmsNucleotide MotifsPhenotypePrognosisProtein BindingAndrogensReceptors, Androgen

Identifiers

PMID27669432
PMCPMC5364060
OpenAlexW2525450724

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.