Evidence map›Paper›PMID 20382258›Full record

ReviewMutation research2010

Toxicogenomic profiling of chemically exposed humans in risk assessment.

Cliona M McHale, Luoping Zhang, Alan E Hubbard, Martyn T Smith

Open access · greenAbstract readReview
In one paragraph

Review in Mutation research, 2010. 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
3.1field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Chemical-Induced Phenotypes at CTD Help Inform the Predisease State and Construct Adverse Outcome Pathways.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    Article
  6. Review
  7. Article
  8. Article
  9. Analysis of the transcriptome in molecular epidemiology studies.Environmental and molecular mutagenesis · 2013
    Review
  10. Article
  11. Review
  12. Article
  13. Moving forward in human cancer risk assessment.Environmental health perspectives · 2011
    Article
  14. Article
  15. Article
  16. 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

4 authors at 1 institution in 1 country.

Cliona M McHaleSchool of Public Health, Divisions of Environmental Health Sciences, and Biostatistics, University of California, Berkeley, CA 94720, USA. cmchale@berkeley.edu
Luoping Zhang
Alan E Hubbard
Martyn T Smith
University of California, Berkeley · US

Funding

Training CoreP42ES004705 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI MORELLO-FROSCH, RACHEL ADELE · 1987 to 2025
$74.6M
BIOMARKERS OF BENZENE EXPOSURE AND GENOTOXICITYR01ES006721 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI SMITH, MARTYN T · 1993 to 2007
$3.3M
NIEHS NIH HHS P42 ES004705NIEHS NIH HHS P42ES04705NIEHS NIH HHS R01 ES006721NIEHS NIH HHS R01ES06721
6 · The paper itself

Abstract

Gene-environment interactions contribute to complex disease development. The environmental contribution, in particular low-level and prevalent environmental exposures, may constitute much of the risk and contribute substantially to disease. Systematic risk evaluation of the majority of human chemical exposures, has not been conducted and is a goal of regulatory agencies in the U.S. and worldwide. With the recent recognition that toxicological approaches more predictive of effects in humans are required for risk assessment, in vitro human cell line data as well as animal data are being used to identify toxicity mechanisms that can be translated into biomarkers relevant to human exposure studies. In this review, we discuss how data from toxicogenomic studies of exposed human populations can inform risk assessment, by generating biomarkers of exposure, early effect, and/or susceptibility, elucidating mechanisms of action underlying exposure-related disease, and detecting response at low doses. Good experimental design incorporating precise, individual exposure measurements, phenotypic anchors (pre-disease or traditional toxicological markers), and a range of relevant exposure levels, is necessary. Further, toxicogenomic studies need to be designed with sufficient power to detect true effects of the exposure. As more studies are performed and incorporated into databases such as the Comparative Toxicogenomics Database (CTD) and Chemical Effects in Biological Systems (CEBS), data can be mined for classification of newly tested chemicals (hazard identification), and, for investigating the dose-response, and inter-relationship among genes, environment and disease in a systems biology approach (risk characterization).

Indexed as

AnimalsArsenicBenzeneEnvironmental ExposureEpigenesis, GeneticFemaleGene Expression ProfilingGenomicsHumansMaleProteomicsRisk AssessmentSystems BiologyToxicogeneticsToxicologyArsenicBenzene

Identifiers

PMID20382258
PMCPMC2928857
OpenAlexW2150862807

What OpenQuestion holds

Textmetadata
LicenceTDM
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.