Monosomie 22 in Ependymomen
Auch gedruckt in der BibliothekZ: J-H 11.453 ; W: W-H 9.561
LizenzStandard (Fassung vom 03.05.2003)
The aim of this study was to investigate the incidence and correlation of a deletion of chromosome 22q in ependymal tumours with clinical features. Archived ependymal tumours were examined by means of fluorescence in situ hybridizing (FISH). It could be shown that FISH is a suitable method to examine archived material of rare tumours and together with comparative genomic hybridization (CGH) opens new ways in tumour genome analysis in paraffin embedded material. So far neither the tumorigenesis of ependymal tumours nor the relevance of cytogenetic changes is elucidated. Comparatively few ependymal tumours were analysed on a molecular cytogenetical level. Instead methods were used like conventional cytogenetics, CGH,, FISH and LOH (loss of heterozygocity). The case numbers in these studies were often very small. In our study, we analysed 67 ependymal tumours, more than in many other studies. Due to the different clinical parameters of the examined ependymal tumours the statistic evaluation was nevertheless difficult. We identified a deletion 22q in 28 of 67 tumours (42%) using FISH. No clear correlation with age, sex, localization or WHO grade could be identified. By means of a logistic regression model with consideration of all variables a subtle influence of sex and localization could be demonstrated in female patients and spinal tumours. In most ependymomas with deletion 22q only in a limited number of nuclei were affected. However no correlation between percentage of nuclei with deletion 22q and clinical parameters such as age, WHO degree, sex and localization could be shown. The relevance of the described gains and losses of genomic material on chromosome 22q for the clinical presentation of ependymal tumours remains unclear and it requires further studies before prognostic statements and optimized therapies can be offered.
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