Meningioma genomics: A therapeutic challenge for clinicians

Abstract

Meningiomas are amongst the most commonly encountered intracranial tumors. The majority of these tumors arise intracranially, and the remaining incidents occur along the spinal cord. Meningiomas tend to grow gradually, with many tumors arising in inaccessible locations. Such sporadic behavior poses a therapeutic challenge to clinicians, causing incomplete tumor resections that often lead to recurrence. Therefore, ongoing research seeks to find alternative systematic treatments for meningiomas, with gene-based therapeutics of high interest. Subsequently, genetic studies characterized frequent somatic mutations in NF2, TRAF7, KLF4, AKT1, SMO, and PIK3CA. These genes are communally exhibited in 80% of sporadic meningiomas. In addition, other genes such as the DUSP family, the NR4 family, CMKOR, and FOSL2, have been identified as key players in spinal meningiomas. In this perspective, we aim to investigate current genetic-based studies, with the ongoing research mainly focused on the above NF2, TRAF7, KLF4, AKT1, SMO, and PIK3CA genes and their involved pathways. In addition, this perspective can serve as a potential cornerstone for future genetic analyses of meningioma cases. © 2021 The Author(s). Published by IMR Press.

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Keywords

Cranial meningioma, Gene-targeting therapy, Genetics, Neurology, Somatic mutations, Spinal meningioma, Humans, Meningeal neoplasms, Meningioma, Antineoplastic agent, Kruppel like factor 4, Merlin, Phosphatidylinositol 3 kinase, Protein, Smoothened protein, Tumor necrosis factor receptor associated factor 7, Unclassified drug, Cancer prognosis, Cell proliferation, Chromosome 22, Chromosome aberration, Dna methylation, Enzyme activation, Epigenetics, Gene deletion, Gene mutation, Genetic analysis, Genomics, Heterozygosity loss, Homozygosity, Human, Intracranial tumor, Nonhuman, Promoter region, Protein analysis, Protein expression, Review, Signal transduction, Tumor growth

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