Evidence map›Paper›PMID 28426665›Full record

ArticlePLoS computational biology2017

Oncodomains: A protein domain-centric framework for analyzing rare variants in tumor samples.

Thomas A Peterson, Iris Ivy M Gauran, Junyong Park, DoHwan Park, Maricel G Kann

Abstract read
In one paragraph

Article in PLoS computational biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Integrating evidence from protein domains to identify cancer driver mutations.Protein science : a publication of the Protein Society · 2026
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  6. Recurrent high-impact mutations at cognate structural positions in class A G protein-coupled receptors expressed in tumors.Proceedings of the National Academy of Sciences of the United States of America · 2021
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  12. Leveraging protein dynamics to identify cancer mutational hotspots using 3D structures.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  13. Article
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  16. Review
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

5 authors.

Thomas A PetersonDepartment of Biological Sciences, University of Maryland, Baltimore County, Baltimore, Maryland, United States of America.
Iris Ivy M GauranDepartment of Mathematics and Statistics, University of Maryland, Baltimore County, Baltimore, Maryland, United States of America.ORCID 0000-0002-7067-7012
Junyong ParkDepartment of Mathematics and Statistics, University of Maryland, Baltimore County, Baltimore, Maryland, United States of America.
DoHwan ParkDepartment of Mathematics and Statistics, University of Maryland, Baltimore County, Baltimore, Maryland, United States of America.ORCID 0000-0002-9132-5040
Maricel G KannDepartment of Biological Sciences, University of Maryland, Baltimore County, Baltimore, Maryland, United States of America.ORCID 0000-0003-0116-3883

Funding

Informatic Profiling of Clinically Relevant MutationR01LM009722 · NLM · UNIVERSITY OF WASHINGTON · PI MOONEY, SEAN DAVID · 2007 to 2014
$3.5M
Protein domains as molecular units to unravel functional pathways of cancer genesK22CA143148 · NCI · UNIVERSITY OF MARYLAND BALTIMORE COUNTY · PI KANN, MARICEL G. · 2009 to 2011
$490k
NCI NIH HHS K22 CA143148NLM NIH HHS R01 LM009722
6 · The paper itself

Abstract

The fight against cancer is hindered by its highly heterogeneous nature. Genome-wide sequencing studies have shown that individual malignancies contain many mutations that range from those commonly found in tumor genomes to rare somatic variants present only in a small fraction of lesions. Such rare somatic variants dominate the landscape of genomic mutations in cancer, yet efforts to correlate somatic mutations found in one or few individuals with functional roles have been largely unsuccessful. Traditional methods for identifying somatic variants that drive cancer are 'gene-centric' in that they consider only somatic variants within a particular gene and make no comparison to other similar genes in the same family that may play a similar role in cancer. In this work, we present oncodomain hotspots, a new 'domain-centric' method for identifying clusters of somatic mutations across entire gene families using protein domain models. Our analysis confirms that our approach creates a framework for leveraging structural and functional information encapsulated by protein domains into the analysis of somatic variants in cancer, enabling the assessment of even rare somatic variants by comparison to similar genes. Our results reveal a vast landscape of somatic variants that act at the level of domain families altering pathways known to be involved with cancer such as protein phosphorylation, signaling, gene regulation, and cell metabolism. Due to oncodomain hotspots' unique ability to assess rare variants, we expect our method to become an important tool for the analysis of sequenced tumor genomes, complementing existing methods.

Indexed as

Computational BiologyDatabases, ProteinEpidermal Growth FactorHumansMitochondrial ProteinsModels, MolecularMutationNeoplasmsOncogene ProteinsProtein BindingProtein Domainsras ProteinsEpidermal Growth FactorMitochondrial ProteinsOncogene ProteinsRAB40AL protein, humanras Proteins

Identifiers

PMID28426665
PMCPMC5398485

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Registered trials

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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.