| Autor: |
Anna Rosati, Silvia Marconi, Bianca Pollo, Alessia Tomassini, Laura Lovato, Emanuela Maderna, Klaus Maier, Andreas Schwartz, Nicolò Rizzuto, Alessandro Padovani, Bruno Bonetti |
| Zdroj: |
Journal of Neuro-Oncology; Jul2009, Vol. 93 Issue 3, p319-324, 6p, 1 Black and White Photograph, 3 Charts |
| Abstrakt: |
Abstract Purpose The hypothesis addressed by this study is that a glutamine synthetase (GS) deficiency in neoplastic astrocytes is a possible molecular basis associated with seizure generation in glioblastoma multiforme (GBM). Methods Quantitative Western blot analysis of GS was performed in 20 individuals operated for malignant glioma. Results The levels of GS in patients with GBM and epilepsy were significantly lower (range 0.04–1.15; mean 0.35 ± 0.36; median 0.25) than in non-epileptic GBM individuals (range 0.78–3.97; mean 1.64 ± 0.99; median 1.25; P = 0.002). No relationship has been found between histological features (i.e. necrosis, gliosis, stroma, inflammatory cells, giant cells, and haemosiderine) and GS expression or epilepsy. Discussion Even though the epileptogenesis in glioma is multifactorial, it is conceivable that a down-regulation of GS may have an important pro-epileptogenic role in GBM, through the slowing of glutamate-glutamine cycle. This study suggests that seizures in GBM are coupled with a highly localized enzyme deficiency. The manipulation of GS activity might constitute a novel principle for inhibiting seizures in patients with glioma epilepsy. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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