Targeted gene expression panel for meningiomas
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA917520 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Targeted gene expression panel for incidental meningiomas
| PRJNA1246501 | ENA
Project description:A previously published custom Nanostring nCounter panel of 75 meningioma related genes and reference genes was performed on human FFPE meningioma samples. This was done as part of a study of the molecular architecture of incidental meningiomas.
2026-04-09 | GSE293815 | GEO
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:Primary outcome(s): Gene expression of targeted genes
| 2625389 | ecrin-mdr-crc
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.
2010-11-30 | GSE16581 | GEO
Project description:Specific gene expression signatures of low grade meningiomas
| PRJNA914288 | ENA
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: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:Correlate the gene expression profiles with the most relevant patterns of chromosome abnormalities (cytogenetic subgroups of meningiomas) and the gene expression profiles could help to explain the differences in clinical behaviour of meningiomas.
2013-01-05 | GSE43290 | 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 43 female and 25 male subjects with sporadic meningioma were identified from the UCLA Neuro-oncology Program Tissue Bank through institutional review board approved protocols. 43 tumors were designated "benign" WHO I, 19 tumors were "atypical" WHO II, and 6 were "anaplastic" WHO III. Gene expression analysis was performed on the 68 tumor biopsies.
2010-11-30 | E-GEOD-16581 | biostudies-arrayexpress