Targeted gene expression panel for incidental meningiomas
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE293815 | GEO | 2026/04/09
REPOSITORIES: GEO
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Project description:A custom Nanostring nCounter panel of 100 or 75 meningioma related genes and reference genes was developed, and performed on human frozen and FFPE meningioma samples. This was done as part of a study developing and validating a targeted gene expression biomarker for meningioma outcomes after surgey and benefit from raditherapy.
2023-09-06 | GSE222054 | GEO
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:Targeted gene expression panel for incidental meningiomas
| PRJNA1246501 | ENA
Project description:We report genomic analysis of 300 meningiomas, the most common primary brain tumors, leading to the discovery of mutations in TRAF7, a proapoptotic E3 ubiquitin ligase, in nearly one-fourth of all meningiomas. Mutations in TRAF7 commonly occurred with a recurrent mutation (K409Q) in KLF4, a transcription factor known for its role in inducing pluripotency, or with AKT1(E17K), a mutation known to activate the PI3K pathway. SMO mutations, which activate Hedgehog signaling, were identified in ~5% of non-NF2 mutant meningiomas. These non-NF2 meningiomas were clinically distinctive-nearly always benign, with chromosomal stability, and originating from the medial skull base. In contrast, meningiomas with mutant NF2 and/or chromosome 22 loss were more likely to be atypical, showing genomic instability, and localizing to the cerebral and cerebellar hemispheres. Collectively, these findings identify distinct meningioma subtypes, suggesting avenues for targeted therapeutics. Analysis of meningioma gene expression data for each mutation subtype. Includes gene expression data from 75 unique meningiomas and 39 replicates.
2014-05-29 | E-GEOD-58037 | biostudies-arrayexpress
Project description:Meningiomas, one of the most common human brain tumors, are derived from arachnoidal cells associated with brain meninges, usually benign and frequently associated with neurofibromatosis type 2. Here we define a human meningioma-typical miRNA profile and characterize effects of one down-regulated miRNA, miR-200a, on tumor growth. Elevated levels of miR-200a inhibited meningioma cell growth in culture and in a tumor model in vivo. Up-regulation of miR-200a decreased expression of transcription factors, ZEB1 and SIP1, with consequently increased expression of E-cadherin, an adhesion protein associated with cell differentiation. Down-regulation of miR-200a in meningiomas and arachnoidal cells resulted in increased expression of β -catenin and cyclin D1 involved in cell proliferation. miR-200a was found to directly target β -catenin mRNA, thereby inhibiting its translation and blocking β -catenin-Wnt signaling, frequently involved in cancer. A direct correlation was found between down-regulation of miR-200a and up-regulation of β-catenin in human meningioma samples. Thus, miR-200a appears to act as a multi-functional tumor suppressor miRNA in meningiomas through effects on the E-cadherin and β -catenin-Wnt signaling pathways. This reveals a previously unrecognized signaling cascade involved in meningioma tumor development and highlights a novel molecular interaction between miR-200a and Wnt signaling, thereby providing insights into novel therapies for meningiomas. 14 meningioma tumor samples were compared to 3 arachnoidal tissue control samples. Two technical replicates were performed for each sample. Normalization and processing included combining the data from technical replicates. The below table contains quantile-normalized data.
2010-06-24 | E-GEOD-17792 | biostudies-arrayexpress
Project description:Introduction: Meningiomas are the most common primary central nervous system (CNS) tumor in adults, comprising one-third of all primary adult CNS tumors. Although several recent publications have identified molecular alterations in meningioma including characteristic mutations, copy number alterations, and gene expression signatures, our understanding of the drivers of meningioma recurrence is limited. Objective: To identify gene expression signatures of 1p-22q-NF2- meningioma recurrence, with concurrent biallelic inactivation of NF2 and loss of chr1p that are heterogenous but enriched for recurrent meningiomas. Methods: Transcriptomic alterations present in recurrent versus primary 1p-22q-NF2- meningiomas were identified using RNA sequencing (RNA-seq) data in a clinically annotated cohort. Results: Recurrent 1p-22q-NF2- meningiomas were enriched for a newly identified GSTM1 null genotype compared to primary meningiomas that showed variable GSTM1 expression and independent external validation was performed. Conclusions: The GSTM1 null genotype is a novel biomarker of 1p-22q-NF2- meningioma recurrence that resolves heterogeneity in existing meningioma subtypes and may be used to guide future clinical management decisions on extent of treatment to improve patient outcomes.
2024-12-09 | GSE283616 | GEO
Project description:Meningiomas, named for their cell of origin, are the most common intracranial tumors in adults, representing 39% of all primary adult central nervous system tumors. These tumors originate in the meninges, which are the outer three layers of tissue between the skull and the brain that cover and protect the brain just under the skull. Most meningioma tumors (85-90 percent) are categorized as benign, with the remaining 10-15 percent being atypical meningioma or malignant meningioma (cancerous). The word “benign” can be misleading for meningiomas. Depending on location and growth rate, a benign meningioma brain tumor may impinge on vital nerves or compress the brain, causing disability. They may even become life threatening. We describe transcriptional signatures of four most common groups of benign meningiomas. Each subgroup of meningiomas displayed a unique gene expression program identifying signaling pathways potentially implicated in the tumorigenesis. These findings will improve our understanding of meningioma tumorigenesis. Objective: To define gene expression signatures of the most common subtypes of meningiomas to better understand cellular processes and signaling pathways specific for each tumor genotype.
2023-03-10 | GSE221429 | GEO
Project description:RNA Nanostring from human meningioma samples This set of data pertains to RNA extracted from 2mm core punches from the representative FFPE blocks, on which a custom codeset was run.
2023-06-14 | GSE228433 | GEO
Project description:Meningiomas are one of the most common adult brain tumors. For most patients, surgical excision is curative. However, up to 20% recur. Currently, the molecular determinants predicting recurrence and malignant transformation are lacking. We performed global genetic and genomic analysis of 85 meningioma samples of various grades. Copy number alterations were assessed by 100K SNP arrays and correlated with gene expression, proliferation indices, and clinical outcome. In addition to chromosome 22q loss, which was detected in the majority of clinical samples, chromosome 18q and 6q loss significantly predicted recurrence and was associated with anaplastic histology. Five "classes" of meningiomas were detected by gene expression analysis that correlated with copy number alterations, recurrence risk, and malignant histology. These classes more accurately predicted tumor recurrence than Ki-67 index, the gold standard for determining risk of recurrence, and highlight substantial expression heterogeneity between meningiomas. These data offer the most complete description of the genomic landscape of meningiomas and provide a set of tools that could be used to more accurately stratify meningioma patients into prognostic risk groups. Tumor biopsies from 53 female and 32 male subjects with sporadic meningioma were identified from the UCLA Neuro-oncology Program Tissue Bank through institutional review board approved protocols. 57 tumors were designated "benign" WHO I, 20 tumors were "atypical" WHO II, and 8 were "anaplastic" WHO III. Affymetrix SNP arrays were performed according to the manufacturer's instructions on DNA extracted from flash frozen meningioma tumors.
2011-10-11 | E-GEOD-16583 | biostudies-arrayexpress
Project description:We report RNA sequencing of 185 meningiomas, which are used to interrogate the biology underlying DNA methylation groups of meningioma.
2022-01-10 | GSE183653 | GEO