Epilepsy in glioblastoma multiforme: correlation with glutamine synthetase levels

Rosati, Anna; Marconi, Silvia; Pollo, Bianca; Tomassini, Alessia; Lovato, Laura; Maderna, Emanuela; Maier, Klaus; Schwartz, Andreas; Rizzuto, Nicolo’; Padovani, Alessandro; Bonetti, Bruno

doi:10.1007/s11060-008-9794-z

Cited by 63 publications

(46 citation statements)

References 26 publications

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“…GS is an astrocytic enzyme playing a crucial role in the metabolism of ammonia and in glutamate recycling. Accumulation of extracellular glutamate, due to low expression levels of GS, is believed to be at the origin of seizures that may accompany gliomas [103]. Other studies established a negative correlation between the expression of GS and the degree of histological malignancy in brain tumors [104].…”

Section: Discussionmentioning

confidence: 99%

Metabolic reprogramming in transformed mouse cortical astrocytes: A proteomic study

Bentaïb

Tullio

Chneiweiss

et al. 2015

Journal of Proteomics

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Section: Discussionmentioning

confidence: 99%

Metabolic reprogramming in transformed mouse cortical astrocytes: A proteomic study

Bentaïb

Tullio

Chneiweiss

et al. 2015

Journal of Proteomics

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“…Glutamine synthetase (GS) deficiency in GBM cells may be coupled with epileptogenesis [5]. Lower levels of GS in brain tumor samples are observed in epileptogenic GBMs as compared with non-epileptogenic GBMs, suggesting a down-regulation of GS may have an important pro-epileptogenic role in GBM [5].…”

Section: Intratumoral Pathwaysmentioning

confidence: 99%

“…Lower levels of GS in brain tumor samples are observed in epileptogenic GBMs as compared with non-epileptogenic GBMs, suggesting a down-regulation of GS may have an important pro-epileptogenic role in GBM [5]. Decreased GS results in accumulation of glutamate by tumor cells in the peritumoral fluid [5].…”

Section: Intratumoral Pathwaysmentioning

confidence: 99%

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Gliomas and seizures

et al. 2012

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Glial neoplasms account for nearly 50% of all adult primary brain tumors. They originate from glial cells in the brain and/or spinal cord and include low-grade diffuse astrocytomas, anaplastic-astrocytomas, and glioblastomas. Of all brain tumors, glioblastoma multiforme (GBM) is the most aggressive and is characterized by rapid glial cell growth, resistance to radio- and chemo- therapies, and relentless infiltration and spreading throughout the central nervous system (CNS). In glioblastomas, primary tumor growth and CNS invasion are associated with the activation of complex structural molecular and metabolic changes within the tumor tissue, which profoundly affect the surrounding neuronal networks and may in part explain induction of epilepsy. In fact, epileptic seizures are very common among patients with glial tumors, reaching nearly 50% in glioblastoma patients and almost 90% in low-grade astrocytomas. The overall hypothesis presented here discusses the possibility that the aberrant tumor cell metabolism may act directly on neuronal network, and this leads to seizure susceptibility. Further invasion and growth of the malignant glial cells exacerbate this initial pathologic state which promotes recurrent seizures (epileptogenesis).

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“…Also, downregluation of glutamine synthetase has been shown in GBM associated with epilepsy as compared to GBM without epilepsy (Rosati, Marconi et al 2009) and it should be reminded that disruption of the BBB per se could induce epileptic seizures (Marchi, Angelov et al 2007). Thus, convergences of different pathways appear to lead to seizure, and interventions should target each of them.…”

Section: Figure 2 About Herementioning

confidence: 99%

Brain tumor epilepsy: A reappraisal and six remaining issues to be debated

Vercueil

2011

Revue Neurologique

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Epilepsy associated with brain tumors presents with specific features deserving medical attention : 1) although commonly reported in patients with brain tumor, either as revealing mode or as a remote complication, limited knowledge is available regarding their epidemiology, clinical evolution, surgical outcome, physiopathology and treatment, providing only clues for clinical management. 2) seizures appear even more threatening for patients and care-givers, providing seizures could meant tumor progression and recurrence. This factor adds to the negative impact epilepsy carry on quality of life measures. 3) pharmacotherapy is complicated by the use of chemotherapy and interaction between antiepileptic drugs and antineoplastic agents are frequent and potentially harmful. 4) the high incidence of epilepsy enlights the question of prophylaxy with antiepileptic drugs, in patients without seizures, or during the perioperative period, and after surgery, when gross total resection has been achieved. This article attempts to provide the reader with an overview of brain tumor epilepsy in its specific aspects and to comment on some remaining issues.

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Epilepsy in glioblastoma multiforme: correlation with glutamine synthetase levels

Cited by 63 publications

References 26 publications

Metabolic reprogramming in transformed mouse cortical astrocytes: A proteomic study

Metabolic reprogramming in transformed mouse cortical astrocytes: A proteomic study

Gliomas and seizures

Brain tumor epilepsy: A reappraisal and six remaining issues to be debated

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