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<p>Glioblastoma (GBM) is the most prevalent and aggressive primary brain tumor. Tumor-associated epilepsy is a clinical challenge in GBM patients, with seizures being a common symptom and reflecting complex interactions within the tumor microenvironment. This review highlights key molecular mechanisms behind GBM-associated epilepsy, including genetic alterations, increased glutamate release, ion channel dysfunction, and inflammation. These factors disrupt the surrounding neurons, promoting seizures. Shared pathways between epilepsy and GBM, such as those involved in synaptic signaling and immune responses, present potential therapeutic targets. Antiseizure drugs remain the primary treatment, with newer options like perampanel showing promise in reducing seizures and possibly influencing tumor growth. Understanding the interplay between epilepsy and GBM at the molecular level is crucial for advancing personalized treatment strategies and improving outcomes for patients.</p>

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The molecular landscape of glioblastoma-associated epilepsy

  • 期刊论文

  • 发表日期：

    2025年6月27日

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  • Thamiris Becker Scheffel,
  • Fernando Mendonça Diz,
  • Andréa Wieck,
  • Karine Rech Begnini,
  • Jaderson Costa da Costa

摘要

Glioblastoma (GBM) is the most prevalent and aggressive primary brain tumor. Tumor-associated epilepsy is a clinical challenge in GBM patients, with seizures being a common symptom and reflecting complex interactions within the tumor microenvironment. This review highlights key molecular mechanisms behind GBM-associated epilepsy, including genetic alterations, increased glutamate release, ion channel dysfunction, and inflammation. These factors disrupt the surrounding neurons, promoting seizures. Shared pathways between epilepsy and GBM, such as those involved in synaptic signaling and immune responses, present potential therapeutic targets. Antiseizure drugs remain the primary treatment, with newer options like perampanel showing promise in reducing seizures and possibly influencing tumor growth. Understanding the interplay between epilepsy and GBM at the molecular level is crucial for advancing personalized treatment strategies and improving outcomes for patients.