Evidence map›Paper›PMID 28349193›Full record

ArticleArchives of toxicology2017

Time-matched analysis of DNA adduct formation and early gene expression as predictive tool for renal carcinogenesis in methylazoxymethanol acetate treated Eker rats.

Valentina Klaus, Heinke Bastek, Katja Damme, Leonard B Collins, Roland Frötschl, Norbert Benda, Dominik Lutter, Heidrun Ellinger-Ziegelbauer, James A Swenberg, Daniel R Dietrich and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Archives of toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. 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

11 authors at 7 institutions in 2 countries.

Valentina KlausComputational Discovery Research, Institute for Diabetes and Obesity, Helmholtz Diabetes Center & German Center for Diabetes Research (DZD), Helmholtz Zentrum München, Neuherberg, Germany.
Heinke BastekHuman and Environmental Toxicology, University of Konstanz, Konstanz, Germany.
Katja DammeDepartment of Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
Leonard B CollinsDepartment of Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
Roland FrötschlFederal Institute for Drugs and Medical Devices, Bonn, Germany.
Norbert BendaFederal Institute for Drugs and Medical Devices, Bonn, Germany.
Dominik LutterComputational Discovery Research, Institute for Diabetes and Obesity, Helmholtz Diabetes Center & German Center for Diabetes Research (DZD), Helmholtz Zentrum München, Neuherberg, Germany.
Heidrun Ellinger-ZiegelbauerInvestigational Toxicology, DD-ED-Toxicology, Bayer AG, Wuppertal, Germany.
James A SwenbergDepartment of Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
Daniel R DietrichHuman and Environmental Toxicology, University of Konstanz, Konstanz, Germany.
Kerstin StemmerMetabolism and Cancer, Institute for Diabetes and Obesity, Helmholtz Diabetes Center & German Center for Diabetes Research (DZD), Helmholtz Zentrum München, Neuherberg, Germany. kerstin.stemmer@helmholtz-muenchen.de.
University of North Carolina at Chapel Hill · USFederal Institute for Drugs and Medical Devices · DEUniversity of Konstanz · DEBayer (Germany) · DEDeutsches Diabetes-Zentrum e.V. · DEGerman Center for Diabetes Research · DEHelmholtz Zentrum München · DE

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Stephanie Engel · 2001 to 2026
$36.3M
NIEHS NIH HHS P30 ES010126
6 · The paper itself

Abstract

Genotoxic carcinogens pose great hazard to human health. Uncertainty of current risk assessment strategies and long latency periods between first carcinogen exposure and diagnosis of tumors have raised interest in predictive biomarkers. Initial DNA adduct formation is a necessary step for genotoxin induced carcinogenesis. However, as DNA adducts not always translate into tumorigenesis, their predictive value is limited. Here we hypothesize that the combined analysis of pro-mutagenic DNA adducts along with time-matched gene expression changes could serve as a superior prediction tool for genotoxic carcinogenesis. Eker rats, heterozygous for the tuberous sclerosis (Tsc2) tumor suppressor gene and thus highly susceptible towards genotoxic renal carcinogens, were continuously treated with the DNA alkylating carcinogen methylazoxymethanol acetate (MAMAc). Two weeks of MAMAc treatment resulted in a time-dependent increase of O

Indexed as

AnimalsCell ProliferationCell Transformation, NeoplasticDNA AdductsDNA DamageDose-Response Relationship, DrugFemaleGene Expression Regulation, NeoplasticGuanineKidneyMaleMethylazoxymethanol AcetateRats, Mutant StrainsTime Factors7-methylguanineDNA AdductsGuanineMethylazoxymethanol AcetateO-(6)-methylguanineBiomarkers of effectBiomarkers of exposureDNA adductsEker ratKidney cancerMethylazoxymethanol acetate

Identifiers

PMID28349193
PMCPMC5617782
OpenAlexW2603626245

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.