C9380023-11c0-4e9f-9b4a-a47f689aa391 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001008304 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:RNA-sequencing for myeloid inflammation-related genes was conducted on primary tumor samples from patients with IDH-wildtype glioblastoma (GBM) and grade 4 IDH-mutant astrocytoma (G4IMA). In addition, the IDH-wildtype murine glioma cell line GL261 and a strain of IDH-mutant GL261 were also sequenced using the murine counterpart of the RNA-sequencing myeloid innate immunity panel.
2024-05-29 | GSE268118 | GEO
Project description:To understand the diversity of expression states within IDH-mutant astrocytoma tumors, we profiled 6341 cells from 10 tumors by single cell RNA-seq
2017-03-31 | GSE89567 | GEO
Project description:WHO classification for tumors of the central nervous system strongly endorses molecular tests for the precise diagnosis of diffuse gliomas. While alterations in the DNA methylation status of gliomas are already well documented and used in specialised clinical centers to distinguish between brain tumor entities, changes to the epigenetic layer at the level of histone modifications are only poorly characterised. Here, we applied a recently developed data-independent acquisition (DIA) - mass spectrometry method to generate a comprehensive histone epi-proteomic map that documents the abundance of almost all characterized and many uncharacterized histone modifications to a series of IDH-mutant oligodendroglioma and astrocytoma samples. Our analysis documented significant abundance differences in almost one-third of the 144 quantified histone peptides. Among them are lower abundance levels of the polycomb repressive mark H3K27me3 in oligodendroglioma samples compared to astrocytomas. We validated this finding by immunohistochemistry using the C36B11 antibody. Surprisingly, we observed inconsistencies with another widely applied H3K27me3 antibody (07-449), providing a warning flag for immunohistochemistry of brain cancers. An unbiased unsupervised clustering analysis of the proteomic dataset separated the two IDH-mutant glioma subtypes in full accordance to the EPIC DNA methylation classifier and the 1p/19q status. The clustering also revealed at least two histone epi-proteomic subgroups of oligodendroglioma, a feature not observable in the DNA methylation dataset. Our results indicate that histone epi-proteomic profiling at the depth of the current method has the capacity to identify clinically-relevant glioma sub-groups. In addition to being of use for diagnostic purposes, this could also provide novel insights in glioma biology and may identify new therapeutic targets.
2020-01-17 | PXD015151 | Pride
Project description:This multi-site, Phase 1/2 clinical trial is an open-label study to identify the safety, pharmacokinetics, and efficacy of a repeated dose regimen of NEO212 for the treatment of patients with radiographically-confirmed progression of Astrocytoma IDH-mutant, Glioblastoma IDH-wildtype, and the safety, pharmacokinetics and efficacy of a repeated dose regimen of NEO212 when given with select SOC for the treatment of solid tumor patients with radiographically confirmed uncontrolled brain metastasis. The study will have three phases, Phase 1, Phase 2a and Phase 2b.
| 92735 | ecrin-mdr-crc
Project description:The outcome of patients with anaplastic gliomas varies considerably depending on histology and single molecular markers such as codeletion of 1p/19q and mutations of the isocitrate dehydrogenase (IDH) gene. Whether a molecularly-based classification of anaplastic gliomas based on large scale genomic or epigenomic analyses is superior to histopathology, may reflect distinct biological subtypes, predict outcome and guide therapy decisions had yet to be determined. Epigenome-wide DNA methylation analysis, which also allows for the detection of copy-number aberrations, was performed in a cohort of 228 patients with anaplastic gliomas (astrocytomas, oligoastrocytomas and oligodendrogliomas), including 115 patients of the NOA-04 trial. We further compared these tumors with a group of 55 glioblastomas. Unsupervised clustering demonstrated two main groups based on IDH mutation status: CpG island methylator phenotype (CIMP) positive (77.5%) or negative (22.5%). CIMP+ (IDH mutant) tumors showed a further separation based on copy-number status of chromosome arms 1p and 19q, but not based on histopathology. CIMP- (IDH wild type) tumors on the other hand showed hallmark copy-number alterations of glioblastomas. These tumors clustered together with CIMP- glioblastomas without forming separate groups based on WHO grade. There was no Tumor classification based on CIMP and 1p/19q status was significantly associated with survival allowing a better prediction of outcome than the current histopathological classification alone: Patients with CIMP+ tumors with 1p/19q codeletion had the best prognosis, followed by patients with CIMP+ but intact 1p/19q status. Patients with CIMP- anaplastic gliomas had the worst prognosis. Collectively, our data suggest that anaplastic gliomas can be grouped into three molecular subtypes with clear association to underlying biology and clinical outcome based on IDH and 1p/19q status. The data do not provide a molecular basis for the diagnosis of anaplastic oligoastrocytoma. We investigated a subset of 228 anaplastic gliomas using the Illumina 450k methylation array.
2014-06-06 | E-GEOD-58218 | biostudies-arrayexpress
Project description:Oligoastrocytoma (OA) was formerly defined as a mixed glioma exhibiting histological features of both astrocytoma and oligodendroglioma. However, OA has been shown to be attributable to either glioma-type based on its molecular characteristics and was excluded from the glioma classification with the introduction of the integrated diagnosis. Nevertheless, some cases showing genetic features of both oligodendroglioma and astrocytoma have been reported since the integrated diagnosis era, and whether OA exists as a glioma-type remains controversial. All previously reported cases were mixed gliomas with and without 1p/19q-codeletion in the lineage of isocitrate dehydrogenase (IDH) mutant gliomas. Herein, we described a 33-year-old man with a progressive headache. Magnetic resonance imaging showed a large left frontal lobe tumor composed of a cystic component with contrast-enhancing walls and a non-contrast-enhancing solid component. The patient underwent a gross total removal of the tumor. Histologically, the cystic and solid components showed oligodendroglioma and astrocytoma morphology, respectively. Immunohistochemically, IDH1-R132H staining was positive in the cystic component and negative in the solid component. Sanger sequencing confirmed the IDH1-R132H mutation and the C228T mutation in the telomerase reverse transcriptase promoter (TERTp) region in the cystic component, while both IDH1/2 and TERTp were wildtype in the solid component. Fluorescence in situ hybridization revealed 1p/19q-codeletion in both areas. The integrated diagnosis led to the diagnosis of oligoastrocytoma consisting of IDH-mutant 1p/19q-codeleted oligodendroglioma and IDH-wildtype astrocytoma. Furthermore, deoxyribonucleic acid (DNA) extracted separately from each area of formalin-fixed paraffin-embedded specimen revealed a distinct methylation profile. On the other hand, the global DNA copy-number analysis derived from the microarray data showed similar copy-number profiles including 1p/19q-codeletion for both sites. This is the first report of a dual-genotype oligoastrocytoma with IDH-mutant 1p/19q-codeleted oligodendroglioma and IDH-wildtype astrocytoma. This extremely rare case provides profound insight into the process of acquiring genetic abnormalities in the development of glioma.
2025-10-31 | GSE280730 | GEO
Project description:SF11940 snATAC Sequencing.Anaplastic Astrocytoma, IDH-mutant.
Tumor location: Left Frontal. Age: 29. Sex: Male .
| EGAD00001006311 | EGA
Project description:Single cell RNA-seq analysis of IDH-mutant astrocytoma
| PRJNA352580 | ENA
Project description:Oligoastrocytoma consisting of IDH-mutant 1p/19q-codeleted oligodendroglioma and IDH-wildtype astrocytoma
| PRJNA1180111 | ENA
Project description:The outcome of patients with anaplastic gliomas varies considerably depending on histology and single molecular markers such as codeletion of 1p/19q and mutations of the isocitrate dehydrogenase (IDH) gene. Whether a molecularly-based classification of anaplastic gliomas based on large scale genomic or epigenomic analyses is superior to histopathology, may reflect distinct biological subtypes, predict outcome and guide therapy decisions had yet to be determined. Epigenome-wide DNA methylation analysis, which also allows for the detection of copy-number aberrations, was performed in a cohort of 228 patients with anaplastic gliomas (astrocytomas, oligoastrocytomas and oligodendrogliomas), including 115 patients of the NOA-04 trial. We further compared these tumors with a group of 55 glioblastomas. Unsupervised clustering demonstrated two main groups based on IDH mutation status: CpG island methylator phenotype (CIMP) positive (77.5%) or negative (22.5%). CIMP+ (IDH mutant) tumors showed a further separation based on copy-number status of chromosome arms 1p and 19q, but not based on histopathology. CIMP- (IDH wild type) tumors on the other hand showed hallmark copy-number alterations of glioblastomas. These tumors clustered together with CIMP- glioblastomas without forming separate groups based on WHO grade. There was no Tumor classification based on CIMP and 1p/19q status was significantly associated with survival allowing a better prediction of outcome than the current histopathological classification alone: Patients with CIMP+ tumors with 1p/19q codeletion had the best prognosis, followed by patients with CIMP+ but intact 1p/19q status. Patients with CIMP- anaplastic gliomas had the worst prognosis. Collectively, our data suggest that anaplastic gliomas can be grouped into three molecular subtypes with clear association to underlying biology and clinical outcome based on IDH and 1p/19q status. The data do not provide a molecular basis for the diagnosis of anaplastic oligoastrocytoma.
2014-06-06 | GSE58218 | GEO