gms | German Medical Science

56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
3èmes journées françaises de Neurochirurgie (SFNC)

Deutsche Gesellschaft für Neurochirurgie e. V.
Société Française de Neurochirurgie

07. bis 11.05.2005, Strasbourg

Interstitial loss and gain of sequences on chromosome 22 in meningiomas with normal karyotype

Interstitielle Verluste und Gewinne auf Chromosom 22 in Meningeomen mit normalem Karyotyp

Meeting Abstract

  • corresponding author A. Prowald - Neurochirurgische Klinik, Neuroonkologie, Universität des Saarlandes, Homburg/Saar
  • S. Urbschat - Institut für Humangenetik, Universität des Saarlandes, Homburg/Saar
  • R. Ketter - Neurochirurgische Klinik, Neuroonkologie, Universität des Saarlandes, Homburg/Saar
  • E. Meese - Institut für Humangenetik, Universität des Saarlandes, Homburg/Saar
  • K. D. Zang - IGD Saar, Institut für genetische Diagnostik, Homburg/Saar
  • W. I. Steudel - Neurochirurgische Klinik, Neuroonkologie, Universität des Saarlandes, Homburg/Saar

Deutsche Gesellschaft für Neurochirurgie. Société Française de Neurochirurgie. 56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3èmes journées françaises de Neurochirurgie (SFNC). Strasbourg, 07.-11.05.2005. Düsseldorf, Köln: German Medical Science; 2005. Doc11.05.-11.01

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2005/05dgnc0227.shtml

Veröffentlicht: 4. Mai 2005

© 2005 Prowald et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective

In nearly half of sporadic low grade meningiomas no chromosome aberration can be detected. In the majority of the other half chromosome 22 is lost. In higher grade meningiomas this loss is followed by characteristic secondary chromosome aberrations. Regarding the molecular findings in Schwannomas, homozygous loss or mutation of the NF2 gene located on chromosome 22, was supposed also to be the primary event in meningioma development. However, in nearly all high-grade but in only a minority of low grade meningiomas the loss of the NF2 protein is observed. Therefore, both the hypothetical combined heterozygous loss of or inactivation of two or more tumour suppressor genes (at least one of them located on chromosome 22) or the homozygous loss of a regulatory gene on chromosome 22 different from NF2 was discussed.

Methods

In search for microdeletions or/and structural recombinations of chromosome 22 we investigated primary cell cultures of 43 meningiomas by conventional G-banding (26 without, 17 with loss of chromosome 22). 27 tumours were analysed with spectral karyotyping (SKY) and 16 with fluorescence in situ hybridisation (FISH) with DNA probes for the chromosomal regions of 22q11.2, 22q11.23q12.1, 22q12.1 and 22q13.3.

Results

SKY analysis confirmed G-banding data for chromosome 22 and could specify marker chromosomes and translocations containing material from chromosome(s) 22. Confirming our assumption microdeletions on chromosome 22 were detected by FISH in 6/8 cytogenetically non-aberrant meningiomas. Suprisingly, in 2/8 cases we observed gains of the 22q13.3 and in 2/8 gains of the 22q12.1 region.

Conclusions

Here we present first evidence for an uncommon mechanism during early meningioma development at least for a meningioma subgroup: (i) duplication and translocation of sequences from chromosome 22 to different chromosomes. (ii) deletion of the original sequences on chromosome 22, resulting in disomy again (only visible as translocation in metaphase FISH). (iii) loss of chromosome 22.