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.
Highlights
Meningiomas derive from the meninges, the tissue layers that cover the brain and spinal cord
Genomic studies have detected that approximately 80% of sporadic meningiomas have recurrent somatic mutations in Neurofibromin 2 (NF2), TNF receptor-activated factor 7 (TRAF7), Krüppel-like factor 4 (KLF4), AKT1, SMO, and PIK3CA [15, 16]
Meningiomas are devoid of AKT1 and NF2 mutations, which constitute between 1% and 5%, harbor mutations in other genes, such as the SMO gene, coding for smoothened homolog protein
Summary
Meningiomas derive from the meninges, the tissue layers that cover the brain and spinal cord. Unreachable meningiomas are more prone to inadequate and partial resection and/or may display malignant behavior (WHO grade II and III). As such, these tumors are more likely to grow steadily and recur. Genomic studies have detected that approximately 80% of sporadic meningiomas have recurrent somatic mutations in NF2, TRAF7, KLF4, AKT1, SMO, and PIK3CA [15, 16]. These mutations are associated with the histologic subtype, site, and clinical course of the tumor. Ongoing efforts to molecularly characterize tumor cells are still necessary to establish a better understanding of the epidemiology, prognosis, and potential therapies of the disease
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