The integrated multiomic diagnosis of sporadic meningiomas: a review of its clinical implications

Abstract

Introduction Meningiomas are generally considered “benign,” however, these tumors can demonstrate variability in behavior and a surprising aggressiveness with elevated rates of recurrence. The advancement of next-generation molecular technologies have led to the understanding of the genomic and epigenomic landscape of meningiomas and more recent correlations with clinical characteristics and behavior. Methods Based on a thorough review of recent peer-reviewed publications (PubMed) and edited texts, we provide a molecular overview of meningiomas with a focus on relevant clinical implications. Results The identification of specific somatic driver mutations has led to the classification of several major genomic subgroups, which account for more than 80% of sporadic meningiomas, and can be distinguished using noninvasive clinical variables to help guide management decisions. Other somatic genomic modifications, including non-coding alterations and copy number variations, have also been correlated with tumor characteristics. Furthermore, epigenomic modifications in meningiomas have recently been described, with DNA methylation being the most widely studied and potentially most clinically relevant. Based on these molecular insights, several clinical trials are currently underway in an effort to establish effective medical therapeutic options for meningioma. Conclusion As we enhance our multiomic understanding of meningiomas, our ability to care for patients with these tumors will continue to improve. Further biological insights will lead to additional progress in precision medicine for meningiomas.

The multiomic landscape of meningiomas: a review and update

“…A recent review has comprehensively outlined different prognostic alterations in meningiomas [ 3 ]. We will briefly summarize a few of these landmark studies as it relates to more recent work focused on the integration of these alterations across different genomics platforms to develop molecular classification schemes for meningiomas.…”

LncRNA-IMAT1 Promotes Invasion of Meningiomas by Suppressing KLF4/hsa-miR22-3p/Snai1 Pathway

“…Compared with invasive meningiomas, the negative correlation between hsa-miR22-3p and its target protein Snai1 was better maintained in non-invasive meningiomas with lower levels of IMAT1. For many years, meningiomas have been considered to have the pathological characteristics of benign tumors ( Robert et al, 2022 ), but the malignant progression of meningiomas should not be ignored. Although the data used for IMAT1 screening came from 8 invasive meningiomas, the uniformity of the detection indicators in the sample makes us no longer doubt the sample size.…”

Brain Invasion and Trends in Molecular Research on Meningioma

“…They include the following variants: 1) neurofibromatosis-2 ( NF2 ) with or without co-mutation in SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily B, member 1 ( SMARCB1 ); 2) mutations in the WD40 region of TNF Receptor-associated factor 7 ( TRAF7 ), which can occur alone; 3) with a recurrent mutation in Kruppel-like factor 4 ( KLF4K409Q ); 4) mutations in PI3K (phosphoinositide 3-kinase) pathway molecules, including phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha ( PIK3CA ), PIK3R1 , and AKT1E17K ; 5) Hedgehog (HH) signaling molecules (i.e. SMO , suppressor of fused [ SUFU ], PRKAR1A ); 6) recurrent mutations in RNA Polymerase II subunit A ( POLR2AQ403K or L438_H439del); or 7) SMARCE1 mutations [ 49 ].…”