Evidence map›Paper›PMID 24096489›Full record

ArticleOncogene2014

EYA4 is inactivated biallelically at a high frequency in sporadic lung cancer and is associated with familial lung cancer risk.

I M Wilson, E A Vucic, K S S Enfield, K L Thu, Y A Zhang, R Chari, W W Lockwood, N Radulovich, D T Starczynowski, J P Banáth and 21 more

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 56 citations in OpenAlex.

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  15. Integrative Genomic Analyses Identifies GGA2 as a Cooperative Driver of EGFR-Mediated Lung Tumorigenesis.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2019
    Article
  16. Article
  17. Inherited lung cancer syndromes targeting never smokers.Translational lung cancer research · 2018
    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

31 authors at 8 institutions in 2 countries.

I M WilsonIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
E A VucicIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
K S S EnfieldIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
K L ThuIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
Y A ZhangHamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX, USA.
R Chari1] Integrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada [2] Department of Genetics, Harvard Medical School, Boston, MA, USA.
W W Lockwood1] Integrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada [2] National Human Genome Research Institute, Cancer Genetics Branch, Bethesda, MD, USA.
N RadulovichOntario Cancer Institute/Princess Margaret Hospital, Toronto, ON, Canada.
D T StarczynowskiDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Research Foundation, Cincinnati, OH, USA.
J P BanáthIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
M ZhangIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
A PusicIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
M FullerIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
K M LonerganIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
D RowbothamIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
J YeeDepartment of Surgery, Vancouver General Hospital, Vancouver, BC, Canada.
J C EnglishDepartment of Pathology, Vancouver General Hospital, Vancouver, BC, Canada.
T P H BuysIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
S A SelamatDepartment of Biochemistry and Molecular Biology, University of Southern California, Los Angeles, CA, USA.
I A Laird-OffringaDepartment of Biochemistry and Molecular Biology, University of Southern California, Los Angeles, CA, USA.
P LiuMedical College of Wisconsin Cancer Center, Milwaukee, WI, USA.
M AndersonMedical College of Wisconsin Cancer Center, Milwaukee, WI, USA.
M YouMedical College of Wisconsin Cancer Center, Milwaukee, WI, USA.
M S TsaoOntario Cancer Institute/Princess Margaret Hospital, Toronto, ON, Canada.
C J BrownDepartment of Medical Genetics, University of British Columbia, Life Sciences Centre, Vancouver, BC, Canada.ORCID 0000000289590101
K L BennewithIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
C E MacAulayIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
A KarsanIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
A F GazdarHamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX, USA.
S LamIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
W L LamIntegrative Oncology Genetics Unit, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
Occupational Cancer Research Centre · CAMedical College of Wisconsin · USUniversity of Southern California · USOntario Institute for Cancer Research · CASouthwestern Medical Center · USVancouver General Hospital · CACincinnati Children's Hospital Medical Center · USUniversity of British Columbia · CA

Funding

UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
GENETIC EPIDEMIOLOGY OF LUNG CANCERU01CA076293 · NCI · UNIVERSITY OF CINCINNATI · PI ANDERSON, MARSHALL W · 1999 to 2009
$11.5M
Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., TSEVAT, JOEL · 2012 to 2014
$9.9M
Novel Reagents and New Biomarkers for Lung CancerU01CA084971 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GAZDAR, ADI F. · 1999 to 2009
$4.5M
CIHR MOP77903CIHR MOP86731CIHR MOP94867NCATS NIH HHS UL1 TR000077NCI NIH HHS 5U01 CA84971-10NCI NIH HHS P50 CA070907NCI NIH HHS U01 CA076293NCI NIH HHS U01 CA084971NCI NIH HHS U01CA76293
6 · The paper itself

Abstract

In an effort to identify novel biallelically inactivated tumor suppressor genes (TSGs) in sporadic invasive and preinvasive non-small-cell lung cancer (NSCLC) genomes, we applied a comprehensive integrated multiple 'omics' approach to investigate patient-matched, paired NSCLC tumor and non-malignant parenchymal tissues. By surveying lung tumor genomes for genes concomitantly inactivated within individual tumors by multiple mechanisms, and by the frequency of disruption in tumors across multiple cohorts, we have identified a putative lung cancer TSG, Eyes Absent 4 (EYA4). EYA4 is frequently and concomitantly deleted, hypermethylated and underexpressed in multiple independent lung tumor data sets, in both major NSCLC subtypes and in the earliest stages of lung cancer. We found that decreased EYA4 expression is not only associated with poor survival in sporadic lung cancers but also that EYA4 single-nucleotide polymorphisms are associated with increased familial cancer risk, consistent with EYA4s proximity to the previously reported lung cancer susceptibility locus on 6q. Functionally, we found that EYA4 displays TSG-like properties with a role in modulating apoptosis and DNA repair. Cross-examination of EYA4 expression across multiple tumor types suggests a cell-type-specific tumorigenic role for EYA4, consistent with a tumor suppressor function in cancers of epithelial origin. This work shows a clear role for EYA4 as a putative TSG in NSCLC.

Indexed as

Gene SilencingCarcinoma, Non-Small-Cell LungChromosomes, Human, Pair 6DNA MethylationEpigenesis, GeneticGene DeletionGene Expression Regulation, NeoplasticGene FrequencyGenes, Tumor SuppressorGenetic Association StudiesGenetic VariationGenome, HumanHumansLung NeoplasmsPolymorphism, Single NucleotideTrans-ActivatorsEYA4 protein, humanTrans-Activators

Identifiers

PMID24096489
PMCPMC4527534
OpenAlexW2070919286

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.