The Genomic Landscape of Meningiomas

Zhao, Amy; Youngblood, Mark W.; Erson‐Omay, E. Zeynep; Moliterno, Jennifer; Günel, Murat

doi:10.1007/978-3-030-59558-6_4

Cited by 1 publication

(4 citation statements)

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“…NF2-mutated meningiomas demonstrate larger volumes, fibrous or atypical histology, male predominance, and preferentially occur along the cerebral convexities posterior to the coronal suture (Fig. 2) [6,15]. Along the skull base, NF2-mutant meningiomas show lateral to medial gradient, originating along the lateral sphenoid wing, invading the bone [16].…”

Section: Nf2-mutated Meningiomasmentioning

confidence: 99%

“…Copy number variations (CNV), including simple duplications, deletions, or complex rearrangements of genomic regions result in altered transcriptional regulation; tumorigenic CNVs cause deletion of tumor suppressor genes or amplification of oncogenes. The most frequent CNV in sporadic meningiomas is chromosome 22q deletion, which contains NF2 and SMARCB1, among others [15,27]. Abnormalities involving Chromosome 1 are also common, with loss of the short arm (1p) being the second most common chromosomal abnormality, found in 70-80% of atypical meningiomas [28].…”

Section: Somatic Copy-number Variationsmentioning

confidence: 99%

Section: Somatic Copy-number Variationsmentioning

confidence: 99%

“…Other frequent CNVs include chromosome 9p deletion, which contains tumor suppressor genes Cyclin-Dependent Kinase Inhibitor 2A and 2B (CDKN2A/B) [15], and loss of chromosomes 2p, 4p, 6q, 7p, 9p, 10q, 11p, 14q, 17q, and 18q [29][30][31][32][33][34][35][36][37]. Chromosome 2p loss is associated with choroid meningiomas, while anaplastic meningiomas demonstrate chromosome 1p, 6p, 14, and 22q losses [15]. CDKN2A/B mutations are associated with recurrent and aggressive tumors [38,39], multiple copies of chromosome 5 are found in angiomatous meningiomas [36], gains in chromosome 22q are more often found in skull base regions, while losses at 1p, 8p, 14q and 22q correlate with non-skull base locations [33,40].…”

Section: Somatic Copy-number Variationsmentioning

confidence: 99%

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

et al. 2021

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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.

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Section: Nf2-mutated Meningiomasmentioning

confidence: 99%

Section: Somatic Copy-number Variationsmentioning

confidence: 99%