Evidence map›Paper›PMID 31900418›Full record

ArticleNature communications2020

Interpreting pathways to discover cancer driver genes with Moonlight.

Antonio Colaprico, Catharina Olsen, Matthew H Bailey, Gabriel J Odom, Thilde Terkelsen, Tiago C Silva, André V Olsen, Laura Cantini, Andrei Zinovyev, Emmanuel Barillot and 7 more

Open access · goldAbstract readEvaluation Study
In one paragraph

Article in Nature communications, 2020. 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
5.9field-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, 105 citations in OpenAlex.

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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

17 authors at 9 institutions in 7 countries.

Antonio ColapricoInteruniversity Institute of Bioinformatics in Brussels (IB)2, Brussels, Belgium. axc1833@med.miami.edu.
Catharina OlsenInteruniversity Institute of Bioinformatics in Brussels (IB)2, Brussels, Belgium.
Matthew H BaileyDivision of Oncology, Department of Medicine, Washington University in St. Louis, St. Louis, MO, 63110, USA.
Gabriel J OdomDepartment of Public Health Sciences, University of Miami, Miller School of Medicine, Miami, FL, 33136, USA.ORCID http://orcid.org/0000-0003-1341-4555
Thilde TerkelsenComputational Biology Laboratory, and Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, Strandboulevarden 49, 2100, Copenhagen, Denmark.
Tiago C SilvaDepartment of Public Health Sciences, University of Miami, Miller School of Medicine, Miami, FL, 33136, USA.ORCID http://orcid.org/0000-0003-1343-6850
André V OlsenComputational Biology Laboratory, and Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, Strandboulevarden 49, 2100, Copenhagen, Denmark.ORCID http://orcid.org/0000-0003-0845-4632
Laura CantiniInstitut Curie, 26 rue d'Ulm, F-75248, Paris, France.ORCID http://orcid.org/0000-0001-6360-4440
Andrei ZinovyevInstitut Curie, 26 rue d'Ulm, F-75248, Paris, France.ORCID http://orcid.org/0000-0002-9517-7284
Emmanuel BarillotInstitut Curie, 26 rue d'Ulm, F-75248, Paris, France.ORCID http://orcid.org/0000-0003-2724-2002
Houtan NoushmehrDepartment of Genetics, Ribeirão Preto Medical School, University of Sao Paulo, Ribeirão Preto, Brazil.
Gloria BertoliInstitute of Molecular Bioimaging and Physiology of the National Research Council (IBFM-CNR), Milan, Italy.ORCID http://orcid.org/0000-0002-5901-4269
Isabella CastiglioniInstitute of Molecular Bioimaging and Physiology of the National Research Council (IBFM-CNR), Milan, Italy.
Claudia CavaInstitute of Molecular Bioimaging and Physiology of the National Research Council (IBFM-CNR), Milan, Italy.ORCID http://orcid.org/0000-0002-5540-4104
Gianluca BontempiInteruniversity Institute of Bioinformatics in Brussels (IB)2, Brussels, Belgium.
Xi Steven ChenDepartment of Public Health Sciences, University of Miami, Miller School of Medicine, Miami, FL, 33136, USA. steven.chen@med.miami.edu.
Elena PapaleoComputational Biology Laboratory, and Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, Strandboulevarden 49, 2100, Copenhagen, Denmark. elenap@cancer.dk.
Institute of Molecular Bioimaging and Physiology · ITUniversité Libre de Bruxelles · BEUniversity of Miami · USDanish Cancer Society · DKInserm · FRCentre National de la Recherche Scientifique · FRHenry Ford Health System · USJames S. McDonnell Foundation · USNovo Nordisk Foundation · DK

Funding

iPGDAC, An Integrative Proteogenomic Data Analysis Center for CPTACU24CA210954 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ZHANG, BING · 2016 to 2020
$4.9M
Integrative prediction models for metastasis risk in colon cancerR01CA158472 · NCI · VANDERBILT UNIVERSITY · PI BEAUCHAMP, ROBERT DANIEL, CHEN, XI STEVEN · 2012 to 2016
$2.3M
Integrative statistical models for TNBC biomarker discoveryR01CA200987 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI CHEN, XI STEVEN · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA158472NCI NIH HHS R01 CA200987NCI NIH HHS U24 CA210954
6 · The paper itself

Abstract

Cancer driver gene alterations influence cancer development, occurring in oncogenes, tumor suppressors, and dual role genes. Discovering dual role cancer genes is difficult because of their elusive context-dependent behavior. We define oncogenic mediators as genes controlling biological processes. With them, we classify cancer driver genes, unveiling their roles in cancer mechanisms. To this end, we present Moonlight, a tool that incorporates multiple -omics data to identify critical cancer driver genes. With Moonlight, we analyze 8000+ tumor samples from 18 cancer types, discovering 3310 oncogenic mediators, 151 having dual roles. By incorporating additional data (amplification, mutation, DNA methylation, chromatin accessibility), we reveal 1000+ cancer driver genes, corroborating known molecular mechanisms. Additionally, we confirm critical cancer driver genes by analysing cell-line datasets. We discover inactivation of tumor suppressors in intron regions and that tissue type and subtype indicate dual role status. These findings help explain tumor heterogeneity and could guide therapeutic decisions.

Indexed as

Genes, Tumor SuppressorOncogenesComputational BiologyDNA MethylationHumansMutationNeoplasmsSoftware

Identifiers

PMID31900418
PMCPMC6941958
OpenAlexW2998647770

What OpenQuestion holds

Textmetadata
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.