gms | German Medical Science

58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

Differential gene-expression in recurrent glioblastoma multiforme

Differentielle Genexpression in Patienten mit Glioblastoma multiforme

Meeting Abstract

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  • corresponding author D. Krex - Klinik für Neurochirurgie, Universitätsklinik Carl Gustav Carus, Technische Universität Dresden
  • K. Robel - Klinik für Neurochirurgie, Universitätsklinik Carl Gustav Carus, Technische Universität Dresden
  • C. Pilarsky - Klinik für Viszeral, Thorax- und Gefäßchirurgie, Universitätsklinik Carl Gustav Carus, Technische Universität Dresden
  • G. Schackert - Klinik für Neurochirurgie, Universitätsklinik Carl Gustav Carus, Technische Universität Dresden

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocFR.09.02

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2007/07dgnc123.shtml

Veröffentlicht: 11. April 2007

© 2007 Krex 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: Glioblastoma multiforme (GBM) is a morphological and molecular extremely heterogeneous tumor. Recent results indicate that aimed individualized therapeutically approaches are most promising to improve the still miserable prognosis of those patients. Therefore, identification of GBM subgroups is a prerequisite. Consequently, in our study we looked at patients with early versus late tumor recurrences in order to identify molecular markers, which might be associated with those different growth patterns. These markers, in turn could be new therapeutic aims.

Methods: Study population comprised ten pairs each of primary and recurrent tumors occurring within 180 days after initial diagnosis (short-term recurrences, STR) and later than 300 days after initial diagnosis (long-term recurrences, LTR), respectively. Exons 5-8 of the p53 gene and the entire coding region of PTEN were investigated by sequence analysis. EGFR amplification was determined. Loss of heterozygosity (LOH) analysis of markers known to be involved in glioma pathogenesis was performed. A chip-based expression analysis was performed in 6 samples (3 STR, and 3 LTR) using Affymetrix, GeneChip® Human genome U133 Plus 2.0.

Results: p53 mutations are less common in STR than in LTR, while genetic variants of the PTEN gene are more frequent in STR. In STR, p53 and PTEN variants occur in combination, while LTR harbour either p53 or PTEN variants. Clustering after Chip analysis revealed clear differentiation between STR and LTR. Construction of a 6-gene comprising predictor is possible. A set of 53 differentially expressed genes was identified.

Conclusions: STR and LTR can be distinguished by p53 and PTEN mutation status and by gene expression profile. A set of 53 differentially expressed genes needs confirmation whether there might be a suitable marker for therapeutic approaches. Of course, our study sample is rather small, and data need further confirmation.