gms | German Medical Science

56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
3èmes journées françaises de Neurochirurgie (SFNC)

Deutsche Gesellschaft für Neurochirurgie e. V.
Société Française de Neurochirurgie

07. bis 11.05.2005, Strasbourg

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Epigenetic inactivation of SLIT2 is frequently found in malignant gliomas

Epigenetische Inaktivierung von SLIT2 findet sich häufig in malignen Gliomen

Meeting Abstract

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  • corresponding author D. Krex - Department of Neurosurgery, University Hospital Carl-Gustav-Carus, Technical University of Dresden
  • A. Dallol - Section of Medical and Molecular Genetics, University of Birmingham, UK
  • F. Latif - Section of Medical and Molecular Genetics, University of Birmingham, UK
  • G. Schackert - Department of Neurosurgery, University Hospital Carl-Gustav-Carus, Technical University of Dresden

Deutsche Gesellschaft für Neurochirurgie. Société Française de Neurochirurgie. 56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3èmes journées françaises de Neurochirurgie (SFNC). Strasbourg, 07.-11.05.2005. Düsseldorf, Köln: German Medical Science; 2005. DocP159

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2005/05dgnc0427.shtml

Veröffentlicht: 4. Mai 2005

© 2005 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 vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.

Gliederung

Text

Objective

The SLIT family (SLIT1-3) consists of large extracellular matrix-secreted and membrane-associated glycoproteins. Slits are essential in axon growth and neural development. In addition, recent reports have shown a frequent epigenetic inactivation by promoter hypermethylation in lung, breast, and colorectal tumours. Here we report on the epigenetic, genetic and expression analysis of SLIT2 in gliomas.

Methods

Seven glioma cell lines, 63 tumour samples from glioma patients and 5 samples from normal tissue were analyzed. Promoter CpG island methylation was analyzed after bisulphite treatment and DNA sequencing. Glioma cell lines were treated with 5-aza-2´-deoxycytidine, and the amount of SLIT2 transcript was investigated using real-time RT-PCR. The amount of SLIT2 mRNA in tumour samples was also determined by real-time PCR. In addition, LOH analysis of the SLIT2 locus at 4p15.2 was performed.

Results

5 out of 7 glioma cell lines and 37 (59%) of all tumour samples were found to be hypermethylated, while SLIT2 was unmethylated in all 5 normal tissues. 5-aza treatment of glioma cell lines could restore SLIT2 expression. LOH was found in only 5% of analyzed cases.

Conclusions

Our data indicate that SLIT2 is frequently inactivated in gliomas by promoter hypermethylation, while this genomic region is no target of frequent loss. Because of its functional properties, SLIT2, located on 4p15.2 might be another candidate for tumour suppressor gene in glioma pathogenesis.