Type of bony involvement predicts genomic subgroup in sphenoid wing meningiomas

Jin, Lan; Youngblood, Mark W.; Gupte, Trisha; Vetsa, Shaurey; Nadar, Arushii; Barak, Tanyeri; Yalçın, Kanat; Aguilera, Stephanie Marie; Mishra-Gorur, Ketu; Blondin, Nicholas; Gorelick, Evan; Omay, Sacit Bulent; Pointdujour-Lim, Renelle; Judson, Benjamin L.; Alperovich, Michael; Aboian, Mariam; McGuone, Declan; Günel, Murat; Erson-Omay, Zeynep; Fulbright, Robert K.; Moliterno, Jennifer

doi:10.1007/s11060-021-03819-2

Cited by 12 publications

(16 citation statements)

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“…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 ]. These mutations are associated with preoperative seizures, predict a more aggressive clinical course, shorter progression free survival [ 17 ], and correlate with higher proliferation indexes [ 6 ].…”

Section: Genomic Landscape Of Sporadic Meningiomasmentioning

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: Genomic Landscape Of Sporadic Meningiomasmentioning

confidence: 99%

“…2 ) [ 6 , 9 ]. Recent data demonstrates that sphenoid wing meningiomas causing hyperostosis are associated with TRAF7 variants [ 16 ].…”

Section: Genomic Landscape Of Sporadic Meningiomasmentioning

confidence: 99%

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

et al. 2021

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“…For example, in sphenoid wing meningiomas, varying grades of bone involvement were associated with different genomic profiles. While bone invasion was associated with NF2 mutations, hyperostosis was seen more often together with TRAF7 aberrations [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Increased proliferation is associated with CNS invasion in meningiomas

et al. 2021

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Introduction Meningiomas are the most common benign intracranial neoplasms. CNS invasion in meningiomas has been integrated into the 2016 WHO classification of CNS tumors as a stand-alone criterion for atypia. Since then, its prognostic impact has been debated based on contradictory results from retrospective analyses. The aim of the study was to elucidate whether histopathological evidence of CNS invasion is associated with increased proliferative potential. Methods We have conducted a quantified measurement of the proliferation marker Ki67 and analyzed its association with CNS invasion determined by histology together with other established prognostic markers of progression. Routine, immunohistochemical staining for Ki67 were digitalized and automatic quantification was done using Image J software. Results Overall, 1718 meningiomas were assessed. Histopathological CNS invasion was seen in 108 cases (6.7%). Uni- and multivariate analysis revealed a significantly higher Ki67 proliferation rate in meningiomas with CNS invasion (p < 0.0001 and p = 0.0098, respectively). Conclusions Meningiomas with histopathological CNS invasion show a higher proliferative activity.

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“…The localization of each tumor was defined according to the position of the center of its attachment in the sphenoid bone. Bone invasion was defined as the presence of enhancing soft tissue within the sphenoid bone on a Magnetic Resonance Imaging (MRI) scan, similar in appearance to the soft tissue enhancement and intensity of intracranial tumors [24]. Hyperostosis was defined as sphenoid wing bone adjacent to the tumor that was thicker than normal cortical bone in Computed Tomography (CT) and MRI scans, with similar CT attenuation.…”

Section: Data Collectionmentioning

confidence: 99%

NF2 Alteration/22q Loss Is Associated with Recurrence in WHO Grade 1 Sphenoid Wing Meningiomas

Sakai

Miyawaki

Teranishi

et al. 2022

Cancers

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Sphenoid wing meningiomas account for 11–20% of all intracranial meningiomas and have a higher recurrence rate than those at other sites. Recent molecular biological analyses of meningiomas have proposed new subgroups; however, the correlation between genetic background and recurrence in sphenoid wing meningiomas has not yet been fully elucidated. In this study, we evaluated the clinical characteristics, pathological diagnosis, and molecular background of 47 patients with sphenoid wing meningiomas. Variants of NF2, AKT1, KLF4, SMO, POLR2A, PIK3CA, TRAF7, and TERT were determined using Sanger sequencing, and 22q loss was detected using multiplex ligation-dependent probe amplification. Alterations were localized at NF2 in 11 cases, had other genotypes in 17 cases, and were not detected in 12 cases. Interestingly, WHO grade 1 meningiomas with NF2 alteration/22q loss (p = 0.008) and a MIB-1 labeling index > 4 (p = 0.03) were associated with a significantly shorter recurrence-free survival, and multivariate analysis revealed that NF2 alteration/22q loss was associated with recurrence (hazard ratio, 13.1). The duration of recurrence was significantly shorter for meningiomas with NF2 alteration/22q loss (p = 0.0007) even if gross-total resection was achieved. Together, these findings suggest that NF2 alteration/22q loss is associated with recurrence in WHO grade 1 sphenoid wing meningiomas.

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Type of bony involvement predicts genomic subgroup in sphenoid wing meningiomas

Cited by 12 publications

References 30 publications

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

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

Increased proliferation is associated with CNS invasion in meningiomas

NF2 Alteration/22q Loss Is Associated with Recurrence in WHO Grade 1 Sphenoid Wing Meningiomas

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