Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA309879 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Experiment: Establishment of expression profiles in grade I and grade II meningiomas and in normal control brain samples. We extracted DNA from specimens and performed mutational analysis in meningiomas and extracted RNA that was processed and hybridized to Affymetrix microarrays.
2016-04-20 | GSE77259 | GEO
Project description:Meningiomas are common brain tumors that are classified into three World Health Organization grades (Grade I: benign, Grade II: atypical and Grade III: malignant) and are molecularly ill-defined tumors. The purpose of this study was identify microRNA (miRNA) molecular signatures unique to the different grades of meningiomas correlating them to prognosis. We have used a miRNA expression microarray to show that meningiomas of all three grades fall into two main molecular groups designated “benign” and “malignant” meningiomas. While all typical meningiomas fall into the benign group and all anaplastic meningiomas fall into the malignant group, atypical meningiomas distribute into either one of these groups. We have identified a miRNA signature that distinguishes benign meningiomas from malignant meningiomas. We studied the gene expression profiles of 340 mammalian miRNAs in 37 primary meningioma tumors by means of DNA microarrays.
2011-01-02 | E-GEOD-19720 | biostudies-arrayexpress
Project description:Meningiomas represent one of the most common and clinically heterogeneous brain tumor types that only modestly correlate with histopathologic features. While emerging molecular profiling efforts have linked specific genomic drivers to distinct clinical patterns, the proteomic landscape of meningiomas remains largely unexplored. We utilize mass spectrometry to profile a clinically well-annotated cohort (n=69) of meningiomas stratified to span all three World Health Organization (WHO) grades and various degrees of clinical aggressiveness. In total, we quantify 3042 unique proteins and compare the patterns across different clinical parameters. Unsupervised clustering analysis highlighted distinct proteomic (n=106 proteins, Welch’s t-test, P<0.01) and pathway-level (e.g. Notch and PI3K/AKT/mTOR) differences between convexity and skull base meningiomas. Supervised comparative analyses of different pathological grades revealed distinct patterns between benign (WHO Grade I) and atypical/malignant (WHO Grade II and III) meningiomas with classic oncogenes often enriched in higher grade lesions. Independent of WHO grade, clinically aggressive meningiomas, that rapidly recurred, also had distinctive protein patterns that converged on mRNA processing and impaired activation of the extracellular matrix naba matrisome complex. Larger sized meningiomas, and those with previous radiation exposure, also had distinct protein profiles. Collectively, we highlight distinct clinically-dependent proteomic patterns of meningiomas that may help better predict outcome and guide the development of more personalized and directed therapies.
2019-05-30 | PXD012923 | Pride
Project description:Meningiomas are common brain tumours arising from meningeal tissue. Despite the majority of them displaying benign features, they can cause mild to severe morbidity. The current main therapeutic approach is complete tumour resection commonly with adjunct radiation therapy. However, tumour location can hamper complete resection and chemotherapies are ineffective. In this study we aim to elucidate dysregulated pathways in meningioma pathogenesis and identify novel molecular targets by deciphering the proteome and phosphoproteome of different grades of meningiomas. Tumour lysates were collected from grade I, II and III frozenmeningioma specimens and three normal healthy human meninges.
2019-01-02 | PXD007073 | Pride
Project description:Meningiomas are common brain tumours arising from meningeal tissue. Despite the majority of them displaying benign features, they can cause mild to severe morbidity. The current main therapeutic approach is complete tumour resection commonly with adjunct radiation therapy. However, tumour location can hamper complete resection and chemotherapies are ineffective. In this study we aim to elucidate dysregulated pathways in meningioma pathogenesis and identify novel molecular targets by deciphering the proteome and phosphoproteome of different grades of meningiomas. Tumour lysates were collected from grade I, II and III frozenmeningioma specimens and three normal healthy human meninges.
2019-01-02 | PXD007125 | Pride
Project description:Meningiomas are common brain tumours arising from meningeal tissue. Despite the majority of them displaying benign features, they can cause mild to severe morbidity. The current main therapeutic approach is complete tumour resection commonly with adjunct radiation therapy. However, tumour location can hamper complete resection and chemotherapies are ineffective. In this study we aim to elucidate dysregulated pathways in meningioma pathogenesis and identify novel molecular targets by deciphering the proteome and phosphoproteome of different grades of meningiomas. Tumour lysates were collected from grade I, II and III frozemeningioma specimens and three normal healthy human meninges.
2019-01-07 | PXD007044 | Pride
Project description:Meningiomas are common brain tumors that are classified into three World Health Organization grades (Grade I: benign, Grade II: atypical and Grade III: malignant) and are molecularly ill-defined tumors. The purpose of this study was identify microRNA (miRNA) molecular signatures unique to the different grades of meningiomas correlating them to prognosis. We have used a miRNA expression microarray to show that meningiomas of all three grades fall into two main molecular groups designated “benign” and “malignant” meningiomas. While all typical meningiomas fall into the benign group and all anaplastic meningiomas fall into the malignant group, atypical meningiomas distribute into either one of these groups. We have identified a miRNA signature that distinguishes benign meningiomas from malignant meningiomas.
2011-01-02 | GSE19720 | GEO
Project description:Meningioma is the most common primary brain tumor in adults, but molecular drivers of progression occurring in a subset of meningiomas are poorly understood. We hypothesized that epigenomic variations are causal for the clinical heterogeneity of meningiomas and may be functionally relevant for disease progression. To test this hypothesis, we performed global DNA methylation profiling of a large cross-sectional cohort and a longitudinal cohort of human meningiomas. Our analysis identifies a DNA hypermethylation signature that is correlated with clinical outcomes and enables more accurate prognostication in intermediate-risk meningiomas than previous classification systems. Analyses of longitudinal high-grade meningioma samples in comparison to clinically benign meningiomas and normal meningeal tissue show convergent contributions, but differing plasticity of copy number variations and DNA hypermethylation along the trajectory of meningioma progression. Systematic analysis of DNA hypermethylation in high-grade meningiomas unravel a tumor suppressive role of clustered protocadherins by regulating b-catenin signaling. Together, our study provides fundamental insights into the molecular mechanisms underlying the heterogeneity of clinically benign and aggressive meningiomas and the microevolutionary adaptation during disease progression.
2026-07-01 | GSE304087 | GEO
Project description:Meningioma is the most common primary brain tumor in adults, but molecular drivers of progression occurring in a subset of meningiomas are poorly understood. We hypothesized that epigenomic variations are causal for the clinical heterogeneity of meningiomas and may be functionally relevant for disease progression. To test this hypothesis, we performed global DNA methylation profiling of a large cross-sectional cohort and a longitudinal cohort of human meningiomas. Our analysis identifies a DNA hypermethylation signature that is correlated with clinical outcomes and enables more accurate prognostication in intermediate-risk meningiomas than previous classification systems. Analyses of longitudinal high-grade meningioma samples in comparison to clinically benign meningiomas and normal meningeal tissue show convergent contributions, but differing plasticity of copy number variations and DNA hypermethylation along the trajectory of meningioma progression. Systematic analysis of DNA hypermethylation in high-grade meningiomas unravel a tumor suppressive role of clustered protocadherins by regulating b-catenin signaling. Together, our study provides fundamental insights into the molecular mechanisms underlying the heterogeneity of clinically benign and aggressive meningiomas and the microevolutionary adaptation during disease progression.
2026-07-01 | GSE304096 | GEO
Project description:Meningioma is the most common primary brain tumor in adults, but molecular drivers of progression occurring in a subset of meningiomas are poorly understood. We hypothesized that epigenomic variations are causal for the clinical heterogeneity of meningiomas and may be functionally relevant for disease progression. To test this hypothesis, we performed global DNA methylation profiling of a large cross-sectional cohort and a longitudinal cohort of human meningiomas. Our analysis identifies a DNA hypermethylation signature that is correlated with clinical outcomes and enables more accurate prognostication in intermediate-risk meningiomas than previous classification systems. Analyses of longitudinal high-grade meningioma samples in comparison to clinically benign meningiomas and normal meningeal tissue show convergent contributions, but differing plasticity of copy number variations and DNA hypermethylation along the trajectory of meningioma progression. Systematic analysis of DNA hypermethylation in high-grade meningiomas unravel a tumor suppressive role of clustered protocadherins by regulating b-catenin signaling. Together, our study provides fundamental insights into the molecular mechanisms underlying the heterogeneity of clinically benign and aggressive meningiomas and the microevolutionary adaptation during disease progression.
2026-07-01 | GSE304094 | GEO