4.3 Article

Clinical significance of astrocyte elevated gene-1 expression in human oligodendrogliomas

Journal

CLINICAL NEUROLOGY AND NEUROSURGERY
Volume 112, Issue 5, Pages 413-419

Publisher

ELSEVIER
DOI: 10.1016/j.clineuro.2010.02.007

Keywords

Astrocyte elevated gene-1; Oligodendroglioma; Tumor progression; Survival

Funding

  1. Nature Science Foundation of China [30770763]
  2. Guangdong Province Nature Science Foundation of China [06021228]

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Objective: To investigate the expression of astrocyte elevated gene-1 (AEG-1) in human oligodendrogliomas and the association between AEG-1 expression and progression of oligodendrogliomas. Methods: The expression of AEG-1 in normal human oligodendroglial cells, oligodendroglioma cell line, and four pairs of matched oligodendroglioma tissues and their adjacent normal brain tissues was detected by quantitative RT-PCR and western blotting. In addition, AEG-1 protein expression was examined in 75 cases of histologically characterized oligodendrogliomas by immunohistochemistry. Statistical analyses were applied to test for prognostic and diagnostic associations. Results: Western blotting and RT-PCR showed that AEG-1 mRNA and protein were elevated in the oligodendroglioma cell line and significantly upregulated in primary oligodendrogliomas compared with the adjacent non-cancerous brain tissues. Immunohistochemical analysis showed that 51 of 75 (68.0%) paraffin-embedded archival oligodendroglioma samples exhibited high expression of AEG-1. Statistical analysis suggested that upregulation of AEG-1 was significantly correlated with the histological grade of oligodendroglioma (p = 0.000) and that patients with high AEG-1 level exhibited shorter survival time (p = 0.000). Multivariate analysis revealed that AEG-1 upregulation might be an independent prognostic indicator for the survival of patients with oligodendroglioma. Conclusions: AEG-1 might represent a novel, useful diagnostic and prognostic marker for oligodendroglioma and play a role during the development and progression of the disease. (C) 2010 Elsevier B.V. All rights reserved.

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