Expression profiling on subclasses of primary parotid gland carcinomas
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Jeannine Meinrath1, Anja Haak2, Nesrin Igci1, Priya Dalvi1,3, Christoph Arolt1, Sonja Meemboor1,4, Udo Siebolts2, Hannah Eischeidt-Scholz1, Claudia Wickenhauser2, Inga Grünewald5, Uta Drebber1,4, Reinhard Büttner1,3,4, Alexander Quaas1,4, Jens-Peter Klußmann4,6, Margarete Odenthal1,3,4, Dirk Beutner6,7 and Moritz Meyer6,8
1 Institute of Pathology, University Hospital of Cologne, Cologne, Germany
2 Department of Pathology, University of Halle, Halle, Germany
3 Center for Molecular Medicine, University of Cologne, Cologne, Germany
4 Center of Integrative Oncology, University Hospital of Cologne, Cologne, Germany
5 Department of Pathology, University Hospital of Münster, Münster, Germany
6 Department of Otorhinolaryngology, Head and Neck Surgery, University of Cologne, Cologne, Germany
7 Department of Otorhinolaryngology, Head and Neck Surgery, University Medical Center Göttingen, Göttingen, Germany
8 Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University Duisburg-Essen, Duisburg, Germany
Keywords: cancer; salivary gland; nanostring; pancancer pathway; gene expression
Received: May 11, 2020 Accepted: October 17, 2020 Published: November 10, 2020
Introduction: The underlying molecular mechanisms of parotid gland carcinomas (PGC) are still unknown. Knowledge about the tumor-driving signaling pathways is necessary either for diagnostics or developing new therapeutic options in this heterogeneous and rare entity.
Material and Methods: 94 matching RNA formalin-fixed and paraffin-embedded tissue samples from PGC and the corresponding non-tumor area, RNA quality and quantity were sufficient for gene expression profiling of 770 genes using the NanoString's nCounter technology. Oncogenic and tumor suppressor genes were examined in the three common PGC tumor entities: adenoid cystic carcinoma (ACC), adenocarcinoma NOS (AC-NOS), and mucoepidermoid carcinoma (MEC).
Results: Expression profiling and subsequent hierarchical cluster analysis clearly differentiated between non-tumor gland tissue samples and PGC. In addition expression pattern of all three entities differed. The extensive pathway analysis proved a prominent dysregulation of the Wnt signaling pathway in the three PGC entities. Moreover, transcript upstream analysis demonstrated a pronounced activation of the PI3K pathway in ACC and MEC.
Discussion: Our findings revealed divergent molecular expression profiles in MEC, ACC and AC-NOS that are presently studied for their potential application in PGC diagnostics. Importantly, identification of Wnt and PI3K signaling in PGC revealed novel options of PGC therapy.
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