EGFR, PIK3CA, KRAS and BRAF mutations in meningiomas

Meningiomas are among the most frequent intracranial tumors. Treatment involves surgical resection with optional subsequent radiotherapy for high-grade meningiomas or radiosurgery following incomplete tumor removal. At present, no pharmacological agents are used as treatment. The use of targeted therapies has been considered, and specific therapies, including anti-EGFR treatment, have been clinically tested. The experience from the treatment of various types of cancers shows that patient outcome depends on the mutational status of particular molecules, including epithelial growth factor receptor (EGFR), Kirsten rat sarcoma viral oncogene homolog (KRAS), v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) and phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit α (PIK3CA). Therefore, the aim of the present study was to assess the occurrence and potential use of these markers in patients with meningioma. In total, 55 formalin-fixed, paraffin-embedded meningioma samples were subjected to genomic sequencing of EGFR (exons 18–21), KRAS (exon 1), BRAF (exon 15) and PI3K (exons 9, 20). No mutations were identified in EGFR, KRAS or BRAF. Point mutations in PIK3CA were revealed in the samples of two patients with atypical and anaplastic meningiomas. Although these mutations appear to be rare, this result, along with previously reported findings, indicates that the PI3K/protein kinase B pathway may serve as a more reasonable molecular target for meningioma than EGFR.