ArticleToxicology and applied pharmacology2020
A toxicogenomic approach for the risk assessment of the food contaminant acetamide.
Article in Toxicology and applied pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 21 citations in OpenAlex.
- Application of a metabolic network-based graph neural network for the identification of toxicant-induced perturbations.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Investigating the dependency of in vitro benchmark concentrations on exposure time in transcriptomics experiments.Toxicology in vitro : an international journal published in association with BIBRA · 2024Article
- State of the Art of Genomic Technology in Toxicology: A Review.International journal of molecular sciences · 2023Review
- Short-term in vivo testing to discriminate genotoxic carcinogens from non-genotoxic carcinogens and non-carcinogens using next-generation RNA sequencing, DNA microarray, and qPCR.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023Review
- A New Method to Overcome Carboxyamide Formation During AFEX Pretreatment of Lignocellulosic Biomass.Frontiers in chemistry · 2021Article
- A Set of Six Gene Expression Biomarkers Identify Rat Liver Tumorigens in Short-term Assays.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetamide (CAS 60-35-5) is detected in common foods. Chronic rodent bioassays led to its classification as a group 2B possible human carcinogen due to the induction of liver tumors in rats. We used a toxicogenomics approach in Wistar rats gavaged daily for 7 or 28 days at doses of 300 to 1500 mg/kg/day (mkd) to determine a point of departure (POD) and investigate its mode of action (MoA). Ki67 labeling was increased at doses ≥750 mkd up to 3.3-fold representing the most sensitive apical endpoint. Differential gene expression analysis by RNA-Seq identified 1110 and 1814 differentially expressed genes in male and female rats, respectively, following 28 days of treatment. Down-regulated genes were associated with lipid metabolism while up-regulated genes included cell signaling, immune response, and cell cycle functions. Benchmark dose (BMD) modeling of the Ki67 labeling index determined the BMD
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Registered trials
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.