Biomarkers related with seizure risk in glioma patients: A systematic review

- Molecules associated with seizure involved in immune responses, synaptic transmission, and cell cycle control in glioma.
- Peritumor region may play a role in the pathomechanisms of glioma patients.
- Inhibitors of potential targets on biomarkers of seizure aetiology and tumour growth should be developed.

Increasing evidence indicates that genetic biomarkers play important roles in the development of glioma-associated seizures. Thus, we performed a systematic review to summarise biomarkers that are associated with seizures in glioma patients. An electronic literature search of public databases (PubMed, Embase and Medline) was performed using the keywords glioma, seizure and epilepsy. A totall of 26 eligible studies with 2224 cases were included in this systematic review of publications to 20 June, 2016. Genetic biomarkers such as isocitrate dehydrogenase 1 (IDH1) mutations, low expression of excitatory amino acid transporter 2 (EAAT2), high xCT expression, overexpression of adenosine kinase (ADK) and low expression of very large G-protein-coupled receptor-1 (VLGR1) are primarily involved in synaptic transmission, whereas BRAF mutations, epidermal growth factor receptor (EGFR) amplification, miR-196b expression and low ki-67 expression are associated with regulation of cell proliferation. However, there is limited evidence regarding the roles of RAD50 interactor 1 (RINT1) and olig2 in epileptogenesis among glioma patients. Glioma-related seizure was related to the dysfunction of tumor microenvironment. Our findings may provide new mechanistic insights into targeted therapy for glioma-related seizures and may result in the development of multi-target therapies.