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57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

German Society for Neuropathology and Neuroanatomy

12. - 15.09.2012, Erlangen

57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

Potential Role of Epithelial to Mesenchymal Transition in Meningioma

Meeting Abstract

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  • presenting/speaker Maren Wallesch - Institut für Neuropathologie, Universitätsklinikum Magdeburg, Magdeburg, Germany
  • Elmar Kirches - Institut für Neuropathologie, Universitätsklinikum Magdeburg, Magdeburg, Germany
  • Christian Mawrin - Institut für Neuropathologie, Universitätsklinikum Magdeburg, Magdeburg, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Erlangen, 12.-15.09.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12dgnnPP3.5

DOI: 10.3205/12dgnn049, URN: urn:nbn:de:0183-12dgnn0496

Published: September 11, 2012

© 2012 Wallesch et al.
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Outline

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Introduction: Epithelial to Mesenchymal Transition (EMT) is a complex process, which enables an epithelial cell to change its phenotype to a mesenchymal one. Despite the known participation of EMT in processes such as gastrulation, it has recently been acknowledged for as a key factor in tumour development. In this study we examine the expression of markers known to be specific for either epithelial or mesenchymal differentiation in human meningiomas.

Methods: Using real-time PCR and western blotting, we studied the expression of three epithelial (Desmoplakin, Zonula-Occludens-1, E-Cadherin) and three mesenchymal (Vimentin, Fibronectin, ß-Catenin) markers in human meningiomas of all three WHO grades. Additionally, meningothelial and fibroblastic WHO grade I tumours were studied separately as examples for either epithelial or mesenchymal phenotype. We also determined expression of the transcription factors SNAIL, SLUG, TWIST and ZEB-1 which are associated with EMT. This data was also correlated to the NF2 status of the tumours.

Results: Comparing 36 WHO grade I and 11 WHO grade II/III tumours, we found a significant (p≤0,05) downregulation of both epithelial and mesenchymal marker mRNA expression in WHO grade II/III tumors. Comparison of meningothelial and fibroblastic meningiomas did not reveal significant expression differences, nor did we found a relation to the NF2 gene status.

Conclusions: Although our findings so far do not correlate with classical EMT, we found a clear downregulation of EMT markers in aggressive meningiomas. Further examinations are necessary to understand the role of EMT and the recently decribed incomplete EMT in meningiomas