Meningiomas are the most common primary intracranial neoplasms in adults. Despite their prevalence, their biologic underpinnings remain incompletely described. The recent application of unbiased next-generation sequencing and epigenomic approaches has implicated a new array of candidate biomarkers and oncogenic drivers. These insights may serve to craft a molecular taxonomy for meningiomas and highlight putative therapeutic targets in an era of biology-informed precision medicine.
Key points
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The natural history of meningiomas is incompletely predicted by their histopathologic grade and treatment history.
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Recurrent somatic mutations in NF2 , TRAF7 , KLF4 , AKT1 , and SMO are collectively present in approximately 80% of sporadic meningiomas, as identified by next-generation sequencing.
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Epigenetic alterations, particularly methylation changes, influence the transcriptional accessibility and consequent expression of a gene, without change in the DNA sequence.
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Epigenetic alterations serve as a complementary strategy for biologic modulation of targeted therapies in meningioma.
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