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68th Annual Meeting of the German Society of Neurosurgery (DGNC)
7th Joint Meeting with the British Neurosurgical Society (SBNS)

German Society of Neurosurgery (DGNC)

14 - 17 May 2017, Magdeburg

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Deletion of chromosome 17q as an important step in the clonal cytogenetic evolution of recurrent meningiomas

Meeting Abstract

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  • Sina Hemmer - Universitätskliniken des Saarlandes, Neurochirurgische Klinik, Homburg/Saar, Deutschland
  • Ralf Ketter - Universitätskliniken des Saarlandes, Neurochirurgische Klinik, Homburg/Saar, Deutschland
  • Steffi Urbschat - Universitätskliniken des Saarlandes, Neurochirurgische Klinik, Homburg/Saar, Deutschland
  • Joachim Oertel - Universitätskliniken des Saarlandes, Neurochirurgische Klinik, Homburg/Saar, Deutschland

Deutsche Gesellschaft für Neurochirurgie. Society of British Neurological Surgeons. 68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 7. Joint Meeting mit der Society of British Neurological Surgeons (SBNS). Magdeburg, 14.-17.05.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocP 029

doi: 10.3205/17dgnc592, urn:nbn:de:0183-17dgnc5920

Published: June 9, 2017

© 2017 Hemmer 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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Objective: Meningiomas are mostly benign tumors that originate from the coverings of the brain and spinal cord. Cytogenetically, most often they reveal a normal karyotype or monosomy of chromosome 22. However, progression of meningiomas is associated by a non-random pattern of secondary losses of other autosomes e.g. deletions of 17q. The aim of this study was to determine the role of chromosome 17q deletions in patients with recurrent meningiomas.

Methods: FISH for chromosome 17q was performed on 22 meningioma biopsies (1 WHO I-,13 WHO II-, 8 WHO III-Tumors) out of 7 patients (4 males, 3 females, mean age: 45,43 years at the date of surgery) that underwent surgery from 1999 to 2015. At least two different tumors of each patient were examined by FISH to evaluate the clonal cytogenetic evolution of recurrent meningiomas. A comparison to former cytogenetic results revealed by CGH- or conventional karyotype analysis, in 10/22 cases, were done.

Results: In all but two cases, the tumor samples showed a significant loss of chromosome 17q (10%-68.5%). Only 1/10 (10%) CGH or karyotyping results showed a loss of chromosome 17. Despite our presumption of being a late event in tumor progression, loss of chromosome 17q was present also in the patients’ early tumor specimens. The percentage of losses displays to first increase over time and then to decrease in the subsequent tumor samples.

Conclusion: Deletion of the long arm of chromosome 17 does not appear to be a late event in meningioma progression. However, we could show that the loss of chromosome 17 seems to be a potential marker for meningioma recurrence that is not detectable by the standard cytogenetic analyses.