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Joint-Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN) and the Scandinavian Neuropathological Society (SNS)

German Society for Neuropathology and Neuroanatomy

22.09.-24.09.2016, Hamburg

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The putative oncogene CPI-17 is up-regulated in schwannoma

Meeting Abstract

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  • presenting/speaker Christian Hagel - University Medical Center Hamburg-Eppendorf, Hamburg, Germany
  • Carsten Dornblut - Leibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany
  • Alexander Schulz - Leibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany
  • Ulrike Wiehl - Leibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany
  • Reinhard E. Friedrich - University Medical Center Hamburg-Eppendorf, Hamburg, Germany
  • Torge Huckhagel - University Medical Center Hamburg-Eppendorf, Hamburg, Germany
  • Victor-Felix Mautner - University Medical Center Hamburg-Eppendorf, Hamburg, Germany
  • Helen Morrison - Leibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. Scandinavian Neuropathological Society. Joint-Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN) and the Scandinavian Neuropathological Society (SNS). Hamburg, 22.-24.09.2016. Düsseldorf: German Medical Science GMS Publishing House; 2016. Doc16dgnnP34

doi: 10.3205/16dgnn38, urn:nbn:de:0183-16dgnn386

Published: September 14, 2016

© 2016 Hagel et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

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Question: Protein kinase C potentiated inhibitor (CPI-17) was previously described to act as an oncoprotein in the merlin pathway. The myosin phosphatase and its substrate merlin are part of a tumour suppressor cascade that can be blocked in two ways, by mutation of the NF2 gene encoding the tumour suppressor protein merlin and by up-regulation of the specific myosin phosphatase inhibitor CPI-17. Inactivation of the merlin tumour suppressor pathway is thought to be a major principle of transformation by CPI-17, the relevance of this oncogenic pathway in the human peripheral nervous system (PNS) is not known.

Methods: CPI-17 expression was screened immunohistochemically in 28 samples of peripheral nerves with non-tumorous pathology and in 160 peripheral nervous system tumours (PNST), including perineurioma, ganglioneuroma, Schwannoma of different aetiology, neurofibromatosis 1-associated neurofibroma and malignant peripheral nerve sheath tumour (MPNST).

Results: CPI-17 was demonstrated in 39/43 schwannomas, whereas all other PNST were CPI-17-negative, except for the perineurioma and two MPNST with mesenchymal differentiation. NF2-associated schwannomas showed lower levels of CPI-17 than sporadic schwannomas. High levels of CPI-17 were associated with increased proliferation.

Conclusion: CPI-17 was identified as a relevant oncoprotein in schwannoma and as a promising diagnostic marker differentiating between schwannoma and other PNST or non-tumorous peripheral nerve lesions.