Evidence map›Paper›PMID 29846728›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2018

Chemical-Induced Phenotypes at CTD Help Inform the Predisease State and Construct Adverse Outcome Pathways.

Allan Peter Davis, Thomas C Wiegers, Jolene Wiegers, Robin J Johnson, Daniela Sciaky, Cynthia J Grondin, Carolyn J Mattingly

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. 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
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

27 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Predicting drug outcome of population via clinical knowledge graph.medRxiv : the preprint server for health sciences · 2024
    Article
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  18. Beyond the looking glass: recent advances in understanding the impact of environmental exposures on neuropsychiatric disease.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Review
  19. Article
  20. Deciphering Adverse Outcome Pathway Network Linked to Bisphenol F Using Text Mining and Systems Toxicology Approaches.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
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

7 authors at 1 institution in 1 country.

Allan Peter DavisDepartment of Biological Sciences.
Thomas C WiegersDepartment of Biological Sciences.
Jolene WiegersDepartment of Biological Sciences.
Robin J JohnsonDepartment of Biological Sciences.
Daniela SciakyDepartment of Biological Sciences.
Cynthia J GrondinDepartment of Biological Sciences.
Carolyn J MattinglyDepartment of Biological Sciences.
North Carolina State University · US

Funding

Translational Research Support CoreP30ES025128 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Sue Fenton · 2015 to 2026
$18.3M
The Comparative Toxicogenomics Database (CTD)R01ES014065 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI DAVIS, ALLAN PETER, MATTINGLY, CAROLYN J. · 2006 to 2021
$10.5M
Advancing mechanism-based studies with cross-species chemical-phenotype dataR01ES023788 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI MATTINGLY, CAROLYN J. · 2015 to 2019
$1.6M
NIEHS NIH HHS P30 ES025128NIEHS NIH HHS R01 ES014065NIEHS NIH HHS R01 ES023788
6 · The paper itself

Abstract

The Comparative Toxicogenomics Database (CTD; http://ctdbase.org) is a public resource that manually curates the scientific literature to provide content that illuminates the molecular mechanisms by which environmental exposures affect human health. We introduce our new chemical-phenotype module that describes how chemicals can affect molecular, cellular, and physiological phenotypes. At CTD, we operationally distinguish between phenotypes and diseases, wherein a phenotype refers to a nondisease biological event: eg, decreased cell cycle arrest (phenotype) versus liver cancer (disease), increased fat cell proliferation (phenotype) versus morbid obesity (disease), etc. Chemical-phenotype interactions are expressed in a formal structured notation using controlled terms for chemicals, phenotypes, taxon, and anatomical descriptors. Combining this information with CTD's chemical-disease module allows inferences to be made between phenotypes and diseases, yielding potential insight into the predisease state. Integration of all 4 CTD modules furnishes unique opportunities for toxicologists to generate computationally predictive adverse outcome pathways, linking chemical-gene molecular initiating events with phenotypic key events, adverse diseases, and population-level health outcomes. As examples, we present 3 diverse case studies discerning the effect of vehicle emissions on altered leukocyte migration, the role of cadmium in influencing phenotypes preceding Alzheimer disease, and the connection of arsenic-induced glucose metabolic phenotypes with diabetes. To date, CTD contains over 165 000 interactions that connect more than 6400 chemicals to 3900 phenotypes for 760 anatomical terms in 215 species, from over 19 000 scientific articles. To our knowledge, this is the first comprehensive set of manually curated, literature-based, contextualized, chemical-induced, nondisease phenotype data provided to the public.

Indexed as

Adverse Outcome PathwaysDatabases, FactualPhenotypeAnimalsDrug-Related Side Effects and Adverse ReactionsGene-Environment InteractionGene OntologyHumansToxicogenetics

Identifiers

PMID29846728
PMCPMC6111787
OpenAlexW2806502219

What OpenQuestion holds

Textmetadata
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.