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Updated: Jul 6, 2025
Correlating Gene-specific DNA Methylation Changes with Expression and Transcriptional Activity of Astrocytic KCNJ10 Kir4.1
Published on: September 26, 2015
Epidemiology, Genetics, and DNA Methylation Grouping of Hyperostotic Meningiomas
Gray Umbach1, Edwina B Tran2, Charlotte D Eaton1
1Department of Neurological Surgery, University of California, San Francisco, San Francisco , California , USA.
Background And Objectives:
Meningiomas are the most common primary intracranial tumors and are among the only tumors that can form lamellar, hyperostotic bone in the tumor microenvironment. Little is known about the epidemiology or molecular features of hyperostotic meningiomas.
Methods:
Using a retrospective database of 342 meningiomas treated with surgery at a single institution, we correlated clinical, tumor-related, targeted next-generation DNA sequencing (n = 39 total, 16 meningioma-induced hyperostosis [MIH]), and surgical variables with the presence of MIH using generalized linear models. Meningioma DNA methylation grouping was analyzed on a separate population of patients from the same institution with preoperative imaging studies sufficient for identification of MIH (n = 200).
Results:
MIH was significantly correlated with anterior fossa (44.3% of MIH vs 17.5% of non-MIH were in the anterior fossa P < .001, c 2 ) or skull base location (62.5% vs 38.3%, P < .001, c 2 ) and lower MIB-1 labeling index. Gross total resection was accomplished in 27.3% of tumors with MIH and 45.5% of nonhyperostotic meningiomas ( P < .05, t test). There was no association between MIH and histological World Health Organization grade ( P = .32, c 2 ). MIH was significantly more frequent in meningiomas from the Merlin-intact DNA methylation group ( P < .05). Somatic missense mutations in the WD-repeat-containing domain of the TRAF7 gene were the most common genetic alteration associated with MIH (n = 12 of 15, 80%, P < .01, c 2 ).
Conclusion:
In this article, we show that MIH has a predilection for the anterior skull base and affected tumors are less amenable to gross total resection. We find no association between MIH and histological World Health Organization grade, but show that MIH is more common in the Merlin-intact DNA methylation group and is significantly associated with TRAF7 somatic missense mutations. These data provide a framework for future investigation of biological mechanisms underlying MIH.
Insights
Meningioma-induced hyperostosis (MIH) is linked to anterior skull base tumors and TRAF7 mutations. These tumors are less likely to be fully removed and are more common in the Merlin-intact DNA methylation group.
Area of Science:
- Neurosurgery
- Oncology
- Genetics
Background:
- Meningiomas are common primary brain tumors.
- Meningiomas can cause hyperostosis (bone thickening).
- Epidemiology and molecular features of hyperostotic meningiomas are poorly understood.
Purpose of the Study:
- To investigate the clinical, molecular, and surgical features of meningioma-induced hyperostosis (MIH).
- To identify factors associated with MIH in meningiomas.
Main Methods:
- Retrospective analysis of 342 meningiomas.
- Correlation of clinical, tumor, DNA sequencing, and surgical data with MIH.
- Analysis of DNA methylation in 200 meningiomas.
Main Results:
- MIH is associated with anterior skull base location and lower MIB-1 index.
- Tumors with MIH were less likely to achieve gross total resection.
- MIH is more frequent in the Merlin-intact DNA methylation group and associated with TRAF7 mutations.
Conclusions:
- MIH predilection for the anterior skull base.
- MIH is associated with poorer surgical resection outcomes.
- MIH is linked to specific DNA methylation groups and TRAF7 mutations, guiding future research.
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