High copy number variation burdens in cranial meningiomas from patients with diverse clinical phenotypes characterized by hot genomic structure changes
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ABSTRACT:
PROVIDER: PRJNA615929 | ENA |
REPOSITORIES: ENA
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Project description:Meningiomas, as the most common primary tumor of the central nervous system, are known to harbor genomic aberrations that associate with clinical phenotypes. Here we performed genome-wide genotyping for cranial meningiomas in 383 Chinese patients and identified 9,821 copy number variations (CNVs).
2020-03-28 | GSE147673 | GEO
Project description:Genome-wide genotyping analysis identified copy number variations in cranial meningiomas in Chinese patients, and demonstrated diverse CNV burdens among individuals with diverse clinical features.
2020-04-06 | PRJEB37584 | EVA
Project description: Not available
| S-EPMC7457130 | biostudies-literature
Project description:Spinal meningiomas account for 1.2-12% of all meningiomas and 25-45% of all spinal tumours. About 20% of intracranial, but also 4.6% of spinal meningiomas recur and require additional treatment. The classification of intracranial meningiomas has evolved considerably in recent years and uses genetic [1,2,4] as well as epigenetic parameters [3,5] in order to more precisely predict the patients’ prognosis and to lay the ground for therapeutic regiments that are adapted to the aggressiveness of a patient’s tumor. On the other hand, spinal meningiomas are missing in many of the large cohorts that were gathered for the molecular profiling of meningiomas. Also, they have never been thoroughly analyzed separately, and their classification still relies on histopathological findings solely. We analysed 65 tumour samples from 63 patients, who had histologically proven spinal meningioma to perform genetic and epigenetic profiling. Clinical features are described in Supplementary Table 1, online resource. T-distributed Stochastic Neighbor Embedding (t-SNE) analysis of genome-wide DNA methylation data shows that most spinal meningiomas separate from cranial meningiomas (Fig. 1A&B) and form two distinct clusters.
2022-10-12 | GSE212449 | GEO
Project description:Meningiomas are the most common primary brain tumor. Though typically benign with a low mutational burden, histopathologic analysis has poor predictive value for malignant behavior and there are no proven chemotherapies. Although DNA methylation patterns distinguish subgroups of meningiomas and have higher predictive value for tumor behavior than histologic classification, little is known about differences in DNA methylation between meningiomas and surrounding normal dura tissue. Using multimodal studies of meningioma/dura pairs, we identified 4 distinct DNA methylation patterns. Diffuse DNA hypomethylation of malignant meningiomas readily facilitated their identification from lower grade tumors by unsupervised clustering. All clusters and 12/12 meningioma-dura pairs exhibited hypomethylation of the gene promoters of a module associated with the craniofacial patterning transcription factor FOXC1 and its upstream lncRNA FOXCUT. Furthermore, we identified an epigenetic continuum of increasing hypermethylation of polycomb repressive complex target promoters with increased histopathologic grade suggesting progressive epigenetic dysregulation is associated with increasing tumor aggressiveness. These findings are a starting point for future investigations of the role of epigenetic dysregulation of FOXC1 and cranial patterning genes in early stages of meningioma formation as well as studies of the utility of polycomb inhibitors for treatment of aggressive meningiomas.
2023-06-22 | GSE178139 | GEO
Project description:Meningiomas are the most common primary brain tumor. Though typically benign with a low mutational burden, histopathologic analysis has poor predictive value for malignant behavior and there are no proven chemotherapies. Although DNA methylation patterns distinguish subgroups of meningiomas and have higher predictive value for tumor behavior than histologic classification, little is known about differences in DNA methylation between meningiomas and surrounding normal dura tissue. Using multimodal studies of meningioma/dura pairs, we identified 4 distinct DNA methylation patterns. Diffuse DNA hypomethylation of malignant meningiomas readily facilitated their identification from lower grade tumors by unsupervised clustering. All clusters and 12/12 meningioma-dura pairs exhibited hypomethylation of the gene promoters of a module associated with the craniofacial patterning transcription factor FOXC1 and its upstream lncRNA FOXCUT. Furthermore, we identified an epigenetic continuum of increasing hypermethylation of polycomb repressive complex target promoters with increased histopathologic grade suggesting progressive epigenetic dysregulation is associated with increasing tumor aggressiveness. These findings are a starting point for future investigations of the role of epigenetic dysregulation of FOXC1 and cranial patterning genes in early stages of meningioma formation as well as studies of the utility of polycomb inhibitors for treatment of aggressive meningiomas.
2023-06-22 | GSE176457 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE16581: Genomic landscape of meningiomas: gene expression GSE16583: Genomic landscape of meningiomas: genotyping Refer to individual Series
2010-12-01 | E-GEOD-16584 | biostudies-arrayexpress
Project description:Background: The prevalence of incidentally discovered meningiomas is increasing. Clinical and radiographic models help predict growth patterns and need for intervention, but there is an unmet need to understand the molecular architecture of incidental meningiomas to improve risk stratification and guide treatment planning. Methods: A cohort of incidental meningiomas from consecutive patients who presented to a neurosurgical clinic at a single institution were analyzed using serial magnetic resonance imaging volumetrics, IMPACT risk groups, targeted gene expression profiling, DNA methylation profiling, and copy number profiling. All adult patients with asymptomatic, incidental intracranial meningioma on imaging examination were included. Volumetric growth, treatment-free survival, and symptom-free survival from time of detection were compared using the Kaplan-Meier method, Cox proportional hazards regression, and competing risks regression analyses. Results: The study cohort was comprised of 238 consecutive incidental meningiomas, 81% from women with a median age at detection of 59 years. Median meningioma volume at detection was 3.83 cm3, median annual and percent volumetric growth rate were 0.3 cm3 and 19.7%, respectively, median volumetric doubling time was 4.3 years, and the median clinical and MRI follow-up were 9.1 and 6.7 years, respectively. The rate of symptomatic progression was 15.5%, and 93.7% of incidental meningiomas were treated during follow-up, with a median time-to-treatment of 1.06 years. IMPACT risk groups stratified treatment-free (p<0.0001) and symptom-free survival (p=0.0007), and only 5% of incidental meningiomas recurred after treatment. Targeted gene expression profiling and DNA methylation profiling revealed that most incidental meningiomas were low molecular risk, although incidental meningiomas from the Hypermitotic DNA methylation group were larger at the time of detection (p=0.0237). Cell cycle genes were suppressed in incidental meningiomas compared to 1434 previously-published non-incidental meningiomas, and incidental meningiomas showed lower copy number alteration burden and distinct patterns of chromosomal alteration compared to non-incidental meningiomas. Molecular high-risk incidental meningiomas had favorable postoperative outcomes compared to propensity-matched non-incidental meningiomas from the same molecular groups. Conclusions: Incidental meningiomas have excellent clinical outcomes after treatment but are overwhelmingly molecularly low risk and slow growing. These data indicate that the majority of incidental meningiomas can be safely followed with serial imaging surveillance. Molecular profiling of incidental meningiomas sheds light on early stages of meningeal tumorigenesis and suggests that early treatment of appropriately selected patients may improve long-term clinical outcomes for molecularly high-risk incidental meningiomas.
2026-04-09 | GSE293851 | GEO
Project description:Proteomics data of endothelial meningiomas, fibrous meningiomas and anaplastic meningiomas
2022-03-17 | PXD032342 |