Artikel
Is molecular cytogenetic diagnostic a solid tool to classify the several glioma subtypes?
Molekularzytogenetische Diagnostik – eine Methode zur Klassifizierung unterschiedlicher Gliom-Subtypen?
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Autoren
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M. Schmitt
- Neurochirurgische Klinik, Universitätskliniken des Saarlandes, Homburg/Saar, Deutschland
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R. Ketter
- Neurochirurgische Klinik, Universitätskliniken des Saarlandes, Homburg/Saar, Deutschland
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S. Wemmert
- Neurochirurgische Klinik, Universitätskliniken des Saarlandes, Homburg/Saar, Deutschland
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S. Urbschat
- Neurochirurgische Klinik, Universitätskliniken des Saarlandes, Homburg/Saar, Deutschland
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W. I. Steudel
- Neurochirurgische Klinik, Universitätskliniken des Saarlandes, Homburg/Saar, Deutschland
| Veröffentlicht: | 11. April 2007 |
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Gliederung
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Objective: In the last few years many studies were published suggesting that the several glioma subtypes are characterized by specific chromosomal alterations. These are cytogenetic aberrations such as losses of the chromosomal regions 1p36 and 19q in oligodendrogliomas, gains of chromosome 7 as well as losses of chromosome 10 in glioblastomas (WHO-grade IV), including the fact that astrocytomas WHO-grade I to III show more changes of the chromosomes 7 and 10 by getting more undifferentiated and therefore more malignant. This study is aimed at finding out if these cytogenetic distinctive features and differences could be used to classify the different glioma subtypes.
Methods: 51 gliomal tumors including 12% oligodendrogliomas (67% WHO-grade II, 33%, WHO-grade III), 14% pilocytic astrocytomas, 4% astrocytomas WHO-grade II, 4% ependymomas, 8% oligoastrocytomas (33% WHO-grade II, 66%, WHO-grade III) and 57% glioblastomas were examined by fluorescence in situ hybridization using centromere specific probes for the chromosomes 7 and 10 and locus specific probes for 1p36 and and the telomere region of 19q.
Results: 48% of the examined glioblastomas showed gains of chromosome 7, 72% losses of chromosome 10 and 20% a combination of both alterations. The FISH-evaluation of pilocytic astrocytomas revealed losses of 1p36 (14%) and 19q (43%). 50% of astrocytomas WHO-grade II show losses of 1p36, 50% losses of 19q. As far as oligodendrogliomas are concerned, it has to be said that losses of 1p36 (33%) and 19q (50%) occur just as such of chromosome 10 (83%) and gains of chromosome 7 (33%). It's striking that numeral aberrations of the chromosomes 7 and 10 (+7/ -10) in oligodendrogliomas are going up when getting more undifferentiated (when approaching the astrocytic type). Oligodendroglial tumor with losses of chromosome 7 were found as well (20%). Losses of chromosome 10 combined with such of 19q appear especially in glioblastoma multiforme (21%).
Conclusions: Considering the fact that losses of 1p36, 19q, chromosome 10 as well as gains of chromosome 7 vary in the examined tumor entities as well as at the different steps of tumor progression, a tumor classification close to the morphological criteria is necessary.
