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

  • Authors:
    • Alexandra Prowald
    • Silke Wemmert
    • Claudia Biehl
    • Simone Storck
    • Thomas Martin
    • Wolfram Henn
    • Ralf Ketter
    • Eckart Meese
    • Klaus D. Zang
    • Wolf-Ingo Steudel
    • Steffi Urbschat
  • View Affiliations

  • Published online on: February 1, 2005     https://doi.org/10.3892/ijo.26.2.385
  • Pages: 385-393
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Abstract

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. 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). Twenty-seven 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. 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. Surprisingly, in 2/8 cases we observed gains of the 22q13.3 and in 2/8 gains of the 22q12.1 region. 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.

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February 2005
Volume 26 Issue 2

Print ISSN: 1019-6439
Online ISSN:1791-2423

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Spandidos Publications style
Prowald A, Wemmert S, Biehl C, Storck S, Martin T, Henn W, Ketter R, Meese E, Zang KD, Steudel W, Steudel W, et al: Interstitial loss and gain of sequences on chromosome 22 in meningiomas with normal karyotype. Int J Oncol 26: 385-393, 2005
APA
Prowald, A., Wemmert, S., Biehl, C., Storck, S., Martin, T., Henn, W. ... Urbschat, S. (2005). Interstitial loss and gain of sequences on chromosome 22 in meningiomas with normal karyotype. International Journal of Oncology, 26, 385-393. https://doi.org/10.3892/ijo.26.2.385
MLA
Prowald, A., Wemmert, S., Biehl, C., Storck, S., Martin, T., Henn, W., Ketter, R., Meese, E., Zang, K. D., Steudel, W., Urbschat, S."Interstitial loss and gain of sequences on chromosome 22 in meningiomas with normal karyotype". International Journal of Oncology 26.2 (2005): 385-393.
Chicago
Prowald, A., Wemmert, S., Biehl, C., Storck, S., Martin, T., Henn, W., Ketter, R., Meese, E., Zang, K. D., Steudel, W., Urbschat, S."Interstitial loss and gain of sequences on chromosome 22 in meningiomas with normal karyotype". International Journal of Oncology 26, no. 2 (2005): 385-393. https://doi.org/10.3892/ijo.26.2.385