gms | German Medical Science

57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

11. bis 14.05.2006, Essen

Specific oncogenes DBCCR1, OLIG2 and IL13RA2 play a role in malignant astrocytoma genesis

Die spezifischen Onkogene DBCCR1, OLIG2 und IL13RA2 spielen auch eine Rolle in der malignen Gliomentwicklung

Meeting Abstract

  • corresponding author O. Bozinov - Neurochirurgische Klinik, Universitätsklinikum Marburg
  • J.-M. Kalk - Neurochirurgische Klinik, Universitätsklinikum Marburg
  • S. Köhler - Neurochirurgische Klinik, Universitätsklinikum Marburg
  • D. Miller - Neurochirurgische Klinik, Universitätsklinikum Marburg
  • H. Bertalanffy - Neurochirurgische Klinik, Universitätsklinikum Marburg
  • U. Sure - Neurochirurgische Klinik, Universitätsklinikum Marburg

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie. Essen, 11.-14.05.2006. Düsseldorf, Köln: German Medical Science; 2006. DocP 06.80

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter:

Veröffentlicht: 8. Mai 2006

© 2006 Bozinov et al.
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Objective: In previous microarray analysis our group detected altered expression levels of the tumour-associated genes DBCCR1, OLIG2 and IL13RA2 in astrocytomas of WHO-grade III and IV. DBCCR1 is frequently targeted by promoter hypermethylation in bladder cancer. OLIG2 plays a key role in the differentiation of motoneurons and oligodendrocytes and regulates the growth of astrocytes. IL13RA2 encodes for one possible subunit of the Interleukin-13 receptor and has been found to be highly expressed in various types of tumours including glioblastomas (GBMs). Further investigations of these specific oncogenetic alterations were performed in these studies on a larger number of tissue samples from astrocytomas of different WHO-grades.

Methods: We utilized semiquantitative two-step RT Real-Time PCR examinations on a total of 40 tissue samples of astrocytomas WHO-grade II to IV and first-time recurrent GBMs after treatment. Analysis was performed using the ABI™ Sequence Detection System ABI PRISM® 7700 and Qiagen™ QuantiTect® SYBR® Green PCR Kits. According to the histological grading the arithmetic mean was calculated and compared.

Results: The highest expression of DBCCR1 was found in the recurrent GBMs compared to primary GBMs (+183%) and astrocytomas grade III (+82%). The lowest expression was detected in astrocytomas grade II. The highest expression of OLIG2 was measurable in grade III astrocytomas, but it was barely detectable in all other grades. The expression of IL13RA2 in the recurrent GBMs was immensely higher as in the primary GBMs (+692%) and considerably in astrocytomas grade III (+57%). It was expressed minor in grade II tumours and significantly lower compared to their next higher grade of tumour (-82%).

Conclusions: The low expression of DBCCR1 in primary GBMs supports the hypothesis of a putative tumour suppressor as described for bladder cancers. Loss of OLIG2 showed higher proliferation of astrocytes in other groups and its low expression in both primary and recurrent GBMs could indicate a possible involvement into the fast growth of these tumours. However, evidence supporting an involvement of this gene in oncogenesis is still controversial. The higher expression levels of IL13RA2 in recurrent GBMs could indicate a protective intrinsic factor against therapy. Our new results in a larger specimen group confirm our previous microarray results and provide further promising data on the expression of the selected oncogenes in different WHO-grade astrocytomas.