Evidence map›Paper›PMID 23393560›Full record

ArticlePloS one2013

Integrated genomic analysis of the 8q24 amplification in endometrial cancers identifies ATAD2 as essential to MYC-dependent cancers.

Maria B Raeder, Even Birkeland, Jone Trovik, Camilla Krakstad, Shyemaa Shehata, Steven Schumacher, Travis I Zack, Antje Krohn, Henrica Mj Werner, Susan E Moody and 11 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.8field-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

47 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
  2. ATAD2 Drives Prostate Cancer Progression to Metastasis.Molecular cancer research : MCR · 2025
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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

21 authors at 5 institutions in 3 countries.

Maria B RaederDepartment of Obstetrics and Gynecology, Haukeland University Hospital, Bergen, Norway. Maria.Rader@uib.no
Even Birkeland
Jone Trovik
Camilla Krakstad
Shyemaa Shehata
Steven Schumacher
Travis I Zack
Antje Krohn
Henrica Mj Werner
Susan E Moody
Elisabeth Wik
Ingunn M Stefansson
Frederik Holst
Anne M Oyan
Pablo Tamayo
Jill P Mesirov
Karl H Kalland
Lars A Akslen
Ronald Simon
Rameen Beroukhim
Helga B Salvesen
University of Bergen · NOBroad Institute · USDana-Farber Cancer Institute · USHaukeland University Hospital · NOUniversity Medical Center Hamburg-Eppendorf · DE

Funding

The Cell-Of-Origin of Human CancersU54CA143798 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI MICHOR, FRANZISKA · 2009 to 2014
$11.2M
Supporting Integrative Genomic Analysis Users with GenePatternR01GM074024 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MESIROV, JILL P. · 2005 to 2019
$6.6M
Knowledge-based Gene Expression Analysis for Biomedical and Cancer ResearchR01CA121941 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MESIROV, JILL P. · 2006 to 2016
$5.1M
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 K08 CA122833NCI NIH HHS K08CA122833NCI NIH HHS R01 CA121941NCI NIH HHS U54 CA143798NCI NIH HHS U54CA143798NIGMS NIH HHS R01 GM074024
6 · The paper itself

Abstract

Chromosome 8q24 is the most commonly amplified region across multiple cancer types, and the typical length of the amplification suggests that it may target additional genes to MYC. To explore the roles of the genes most frequently included in 8q24 amplifications, we analyzed the relation between copy number alterations and gene expression in three sets of endometrial cancers (N = 252); and in glioblastoma, ovarian, and breast cancers profiled by TCGA. Among the genes neighbouring MYC, expression of the bromodomain-containing gene ATAD2 was the most associated with amplification. Bromodomain-containing genes have been implicated as mediators of MYC transcriptional function, and indeed ATAD2 expression was more closely associated with expression of genes known to be upregulated by MYC than was MYC itself. Amplifications of 8q24, expression of genes downstream from MYC, and overexpression of ATAD2 predicted poor outcome and increased from primary to metastatic lesions. Knockdown of ATAD2 and MYC in seven endometrial and 21 breast cancer cell lines demonstrated that cell lines that were dependent on MYC also depended upon ATAD2. These same cell lines were also the most sensitive to the histone deacetylase (HDAC) inhibitor Trichostatin-A, consistent with prior studies identifying bromodomain-containing proteins as targets of inhibition by HDAC inhibitors. Our data indicate high ATAD2 expression is a marker of aggressive endometrial cancers, and suggest specific inhibitors of ATAD2 may have therapeutic utility in these and other MYC-dependent cancers.

Indexed as

Adenosine TriphosphatasesATPases Associated with Diverse Cellular ActivitiesCell Line, TumorDNA-Binding ProteinsEndometrial NeoplasmsFemaleGenes, mycGenomicsHumansImmunoblottingIn Situ Hybridization, FluorescenceAdenosine TriphosphatasesATAD2 protein, humanATPases Associated with Diverse Cellular ActivitiesDNA-Binding Proteins

Identifiers

PMID23393560
PMCPMC3564856
OpenAlexW2131339364

What OpenQuestion holds

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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.