Multicenter study of acetaminophen hepatotoxicity reveals the importance of biological endpoints in genomic analyses.

doi:10.1093/toxsci/kfm150

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Multicenter study of acetaminophen hepatotoxicity reveals the importance of biological endpoints in genomic analyses.

Toxicological sciences : an official journal of the Society of Toxicology - 1 Sept 2007

Beyer Richard P, Fry Rebecca C, Lasarev Michael R, McConnachie Lisa A, Meira Lisiane B, Palmer Valerie S, Powell Christine L, Ross Pamela K, Bammler Theo K, Bradford Blair U, Cranson Alex B, Cunningham Michael L, Fannin Rickie D, Higgins Gregory M, Hurban Patrick, Kayton Robert J, Kerr Kathleen F, Kosyk Oksana, Lobenhofer Edward K, Sieber Stella O, Vliet Portia A, Weis Brenda K, Wolfinger Russel, Woods Courtney G, Freedman Jonathan H, Linney Elwood, Kaufmann William K, Kavanagh Terrance J, Paules Richard S, Rusyn Ivan, Samson Leona D, Spencer Peter S, Suk William, Tennant Raymond J, Zarbl Helmut

Abstract excerpt

Gene expression profiling is a widely used technique with data from the majority of published microarray studies being publicly available. These data are being used for meta-analyses and in silico discovery; however, the comparability of toxicogenomic data generated in multiple laboratories has n...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acetaminophen

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Analgesics, Non-Narcotic

Share to Endpoint Determination

Share to Genomic Islands

Share to Genomics

Share to Isomerism

Share to Liver

Share to Reproducibility of Results

Source

Open in PubMed

Identifiers

PMID: 17562736
DOI: 10.1093/toxsci/kfm150

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-17562736-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Multicenter study of acetaminophen hepatotoxicity reveals the importance of biological endpoints in genomic analyses.PMID 17562736Read ↗

Metabolic phenotyping applied to pre-clinical and clinical studies of acetaminophen metabolism and hepatotoxicity.Semantic proximity Read ↗

The Genomics of Elevated ALT and Adducts in Therapeutic Acetaminophen Treatment: a Pilot Study.Semantic proximity Read ↗

Interindividual variation in gene expression responses and metabolite formation in acetaminophen-exposed primary human hepatocytes.Semantic proximity Read ↗

Expression Profiling of Acetaminophen Liver Toxicity in Mice Using Microarray TechnologySemantic proximity Read ↗

Population-based discovery of toxicogenomics biomarkers for hepatotoxicity using a laboratory strain diversity panel.Semantic proximity Read ↗

Comparative analysis of gene expression between mice and humans in acetaminophen-induced liver injury by integrating bioinformatics analysisSemantic proximity Read ↗

Toxicogenomics-based prediction of acetaminophen-induced liver injury using human hepatic cell systemsSemantic proximity Read ↗

Genomic identification of potential risk factors during acetaminophen-induced liver disease in susceptible and resistant strains of mice.Semantic proximity Read ↗

Deciphering Acetaminophen-Induced Hepatotoxicity: The Crucial Role of Transcription Factors like Nuclear Factor Erythroid 2-Related Factor 2 as Genetic Determinants of Susceptibility to Drug-Induced Liver Injury.Semantic proximity Read ↗

Identification of novel toxicity-associated metabolites by metabolomics and mass isotopomer analysis of acetaminophen metabolism in wild-type and Cyp2e1-null mice.Semantic proximity Read ↗

Genetic Association of Single Nucleotide Polymorphisms with Acetaminophen-Induced Hepatotoxicity.Semantic proximity Read ↗

Mouse population-guided resequencing reveals that variants in CD44 contribute to acetaminophen-induced liver injury in humans.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.