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The complex molecular epileptogenesis landscape of glioblastoma

Victoria Soeung1, Ralph B Puchalski2, Jeffrey L Noebels3

  • 1Developmental Neurogenetics Laboratory, Department of Neurology, Baylor College of Medicine, Houston, TX, USA.

Cell Reports. Medicine
|August 21, 2024
PubMed

Insights

Glioblastoma tumors disrupt brain excitability, leading to seizures. Specific epilepsy gene patterns at the tumor edge explain why some patients develop seizures and others don't.

Area of Science:

  • Neuroscience
  • Oncology
  • Genetics

Background:

  • Malignant glioblastoma creates a cortical microenvironment promoting hyperexcitability, tumor growth, and immune evasion.
  • Factors like neosynaptogenesis, excess glutamate, and altered membrane currents contribute to excitability imbalances, but only half of glioblastoma cases develop seizures.

Purpose of the Study:

  • To investigate the role of epilepsy genes in the glioblastoma microenvironment and their correlation with seizure development.
  • To understand the genetic basis of peritumoral hyperexcitability and epileptogenesis in glioblastoma patients.

Main Methods:

  • Analysis of spatial contours and expression of 358 validated human epilepsy genes in glioblastoma transcriptomes.
  • Comparison with non-tumor adult and developing cortex gene expression datasets.

Main Results:

  • Approximately half of the studied epilepsy genes, including dosage-sensitive genes linked to monogenic epilepsy, were significantly enriched and aberrantly regulated at the leading edge of glioblastoma.
  • These findings suggest a complex genetic basis for seizures in the vicinity of brain tumors.

Conclusions:

  • Aberrant expression of epilepsy genes in the glioblastoma microenvironment contributes to peritumoral hyperexcitability and epileptogenesis.
  • This genetic dysregulation may explain the variable occurrence of seizures in glioblastoma patients and the limited efficacy of current treatments.
Keywords:
GBMautoimmune epilepsyepistasisfocal dysplasiahyperexcitabilitymicroenvironmentmonogenic epilepsyproliferationspatial transcriptometumor margin

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