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  Transcriptomic responses generated by hepatocarcinogens in a battery of liver-based in vitro models

Doktorova, T. Y., Yildirimman, R., Vinken, M., Vilardell, M., Vanhaecke, T., Gmuender, H., et al. (2013). Transcriptomic responses generated by hepatocarcinogens in a battery of liver-based in vitro models. Carcinogenesis, 34(6), 1393-402. doi:10.1093/carcin/bgt054.

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Doktorova.pdf (Verlagsversion), 3MB
 
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2014
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© 2014 Oxford University Press
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Doktorova, T. Y., Autor
Yildirimman, R.1, Autor           
Vinken, M., Autor
Vilardell, M.2, Autor           
Vanhaecke, T., Autor
Gmuender, H., Autor
Bort, R., Autor
Brolen, G., Autor
Holmgren, G., Autor
Li, R., Autor
Chesne, C., Autor
van Delft, J., Autor
Kleinjans, J., Autor
Castell, J., Autor
Bjorquist, P., Autor
Herwig, R.1, Autor           
Rogiers, V., Autor
Affiliations:
1Bioinformatics (Ralf Herwig), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479648              
2Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433550              

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Schlagwörter: Animals Carcinogens/pharmacology/*toxicity Cell Line, Tumor Embryonic Stem Cells/drug effects Gene Expression/drug effects Gene Expression Profiling Hep G2 Cells Hepatocytes/*drug effects Humans Liver/*drug effects Liver Neoplasms Mutagens/pharmacology/*toxicity Rats Rats, Sprague-Dawley Transcriptome/*drug effects Tumor Suppressor Protein p53/drug effects
 Zusammenfassung: As the conventional approach to assess the potential of a chemical to cause cancer in humans still includes the 2-year rodent carcinogenicity bioassay, development of alternative methodologies is needed. In the present study, the transcriptomics responses following exposure to genotoxic (GTX) and non-genotoxic (NGTX) hepatocarcinogens and non-carcinogens (NC) in five liver-based in vitro models, namely conventional and epigenetically stabilized cultures of primary rat hepatocytes, the human hepatoma-derived cell lines HepaRG and HepG2 and human embryonic stem cell-derived hepatocyte-like cells, are examined. For full characterization of the systems, several bioinformatics approaches are employed including gene-based, ConsensusPathDB-based and classification analysis. They provide convincingly similar outcomes, namely that upon exposure to carcinogens, the HepaRG generates a gene classifier (a gene classifier is defined as a selected set of characteristic gene signatures capable of distinguishing GTX, NGTX carcinogens and NC) able to discriminate the GTX carcinogens from the NGTX carcinogens and NC. The other in vitro models also yield cancer-relevant characteristic gene groups for the GTX exposure, but some genes are also deregulated by the NGTX carcinogens and NC. Irrespective of the tested in vitro model, the most uniformly expressed pathways following GTX exposure are the p53 and those that are subsequently induced. The NGTX carcinogens triggered no characteristic cancer-relevant gene profiles in all liver-based in vitro systems. In conclusion, liver-based in vitro models coupled with transcriptomics techniques, especially in the case when the HepaRG cell line is used, represent valuable tools for obtaining insight into the mechanism of action and identification of GTX carcinogens.

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Sprache(n): eng - English
 Datum: 2013-01-152012-08-302013-02-022013-02-072013
 Publikationsstatus: Erschienen
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 Identifikatoren: Anderer: 23393228
DOI: 10.1093/carcin/bgt054
ISSN: 1460-2180 (Electronic)0143-3334 (Linking)
URI: http://www.ncbi.nlm.nih.gov/pubmed/23393228http://carcin.oxfordjournals.org/content/34/6/1393.full.pdf
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Titel: Carcinogenesis
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: London [etc. : IRL Press]
Seiten: - Band / Heft: 34 (6) Artikelnummer: - Start- / Endseite: 1393 - 402 Identifikator: ISSN: 0143-3334
CoNE: https://pure.mpg.de/cone/journals/resource/954925472375