CYP3A5 mediates basal and acquired therapy resistance in different subtypes of pancreatic ductal adenocarcinoma View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-03

AUTHORS

Elisa M Noll, Christian Eisen, Albrecht Stenzinger, Elisa Espinet, Alexander Muckenhuber, Corinna Klein, Vanessa Vogel, Bernd Klaus, Wiebke Nadler, Christoph Rösli, Christian Lutz, Michael Kulke, Jan Engelhardt, Franziska M Zickgraf, Octavio Espinosa, Matthias Schlesner, Xiaoqi Jiang, Annette Kopp-Schneider, Peter Neuhaus, Marcus Bahra, Bruno V Sinn, Roland Eils, Nathalia A Giese, Thilo Hackert, Oliver Strobel, Jens Werner, Markus W Büchler, Wilko Weichert, Andreas Trumpp, Martin R Sprick

ABSTRACT

Although subtypes of pancreatic ductal adenocarcinoma (PDAC) have been described, this malignancy is clinically still treated as a single disease. Here we present patient-derived models representing the full spectrum of previously identified quasi-mesenchymal (QM-PDA), classical and exocrine-like PDAC subtypes, and identify two markers--HNF1A and KRT81--that enable stratification of tumors into different subtypes by using immunohistochemistry. Individuals with tumors of these subtypes showed substantial differences in overall survival, and their tumors differed in drug sensitivity, with the exocrine-like subtype being resistant to tyrosine kinase inhibitors and paclitaxel. Cytochrome P450 3A5 (CYP3A5) metabolizes these compounds in tumors of the exocrine-like subtype, and pharmacological or short hairpin RNA (shRNA)-mediated CYP3A5 inhibition sensitizes tumor cells to these drugs. Whereas hepatocyte nuclear factor 4, alpha (HNF4A) controls basal expression of CYP3A5, drug-induced CYP3A5 upregulation is mediated by the nuclear receptor NR1I2. CYP3A5 also contributes to acquired drug resistance in QM-PDA and classical PDAC, and it is highly expressed in several additional malignancies. These findings designate CYP3A5 as a predictor of therapy response and as a tumor cell-autonomous detoxification mechanism that must be overcome to prevent drug resistance. More... »

PAGES

278-287

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nm.4038

    DOI

    http://dx.doi.org/10.1038/nm.4038

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1018951632

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/26855150


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    608 Institute of Pharmacy and Molecular Biotechnology, Bioquant, University of Heidelberg, Heidelberg, Germany.
    609 National Center for Tumor Diseases (NCT), Heidelberg, Germany.
    610 rdf:type schema:Organization
    611 https://www.grid.ac/institutes/grid.7700.0 schema:alternateName Heidelberg University
    612 schema:name Department of Pathology, University of Heidelberg, Heidelberg, Germany.
    613 rdf:type schema:Organization
     




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