Similar Datasets
Project description:Astrocytoma is a common pathologic type of glioma, its survival and prognosis remain poor.
2019-10-17 | GSE138999 | GEO
Project description:miRNA profiling by array of astrocytic tumors
| PRJNA577098 | ENA
Project description:This study aims at investigating differential gene expression in human diffusely infiltrating astrocytic tumours, grades II, III and IV. A total of 63 tumours were assessed using the Affymetrix U133A GeneChip. Samples comprised in this GEO submission are identical to those in submission GSE1993 with the exception of two pilocytic astrocytoma tumours (grade I) that have not been included. The study aims not only at discovering the main expression differences between astrocytic tumours of distinct histological grades but also wishes to correlate these findings with the known histopathological and biological hallmarks of astrocytoma progression. Further, the study aims at correlating gene expression with previously obtained genomic information for several loci known to be involved in astrocytoma tumour progression. Keywords: other
2007-05-26 | GSE2727 | GEO
Project description:This study aims at investigating differential gene expression in human astrocytic tumours of grades I, II, III and IV. A total of 65 tumours were assessed using the Affymetrix U133A GeneChip. The study aims not only at discovering the main expression differences between astrocytic tumours of distinct histological grades but also wishes to correlate these findings with the known histopathological hallmarks of astrocytoma progression. Further, the study aims at correlating gene expression with previously obtained genomic information for several loci known to be involved in astrocytoma tumour progression. Keywords: other
2007-05-26 | GSE1993 | GEO
Project description:This study aims at investigating differential gene expression in human diffusely infiltrating astrocytic tumours, grades II, III and IV. A total of 63 tumours were assessed using the Affymetrix U133A GeneChip. Samples comprised in this GEO submission are identical to those in submission GSE1993 with the exception of two pilocytic astrocytoma tumours (grade I) that have not been included. The study aims not only at discovering the main expression differences between astrocytic tumours of distinct histological grades but also wishes to correlate these findings with the known histopathological and biological hallmarks of astrocytoma progression. Further, the study aims at correlating gene expression with previously obtained genomic information for several loci known to be involved in astrocytoma tumour progression. Experiment Overall Design: A total of 63 tumours were assessed using the Affymetrix U133A GeneChip.
2008-06-12 | E-GEOD-2727 | biostudies-arrayexpress
Project description:Diffuse gliomas represent the most prevalent class of primary brain tumor. Despite significant recent advances in the understanding of glioblastoma (WHO IV), its most malignant subtype, lower-grade (WHO II and III) glioma variants remain comparatively understudied, especially in light of their notably variable clinical behavior. To examine the foundations of this heterogeneity, we performed multidimensional molecular profiling, including global transcriptional analysis, on 101 lower-grade diffuse astrocytic gliomas collected at our own institution, and validated our findings using publically available gene expression and copy number data from large independent patient cohorts. We found that IDH mutational status delineated molecularly and clinically distinct glioma subsets, with IDH mutant (IDH mt) tumors exhibiting TP53 mutations, PDGFRA overexpression, and prolonged survival, and IDH wild-type (IDH wt) tumors exhibiting EGFR amplification, PTEN loss, and unfavorable disease outcome. Furthermore, global expression profiling revealed three robust molecular subclasses within lower-grade diffuse astrocytic gliomas, two of which were predominantly IDH mt and one almost entirely IDH wt. IDH mt subclasses were distinguished from each other on the basis of TP53 mutations, DNA copy number abnormalities, and links to distinct stages of neurogenesis in the subventricular zone (SVZ). This latter finding implicates discrete pools of neuroglial progenitors as cells of origin for the different subclasses of IDH mt tumors. In summary, we have elucidated molecularly distinct subclasses of lower-grade diffuse astrocytic glioma that dictate clinical behavior and demonstrate fundamental associations with both IDH mutational status and neuroglial developmental stage. 80 tumor samples, one normal tissue sample (brain)
2012-02-24 | E-GEOD-35158 | biostudies-arrayexpress
Project description:This study aims at investigating differential gene expression in human astrocytic tumours of grades I, II, III and IV. A total of 65 tumours were assessed using the Affymetrix U133A GeneChip. The study aims not only at discovering the main expression differences between astrocytic tumours of distinct histological grades but also wishes to correlate these findings with the known histopathological hallmarks of astrocytoma progression. Further, the study aims at correlating gene expression with previously obtained genomic information for several loci known to be involved in astrocytoma tumour progression.
2008-06-12 | E-GEOD-1993 | biostudies-arrayexpress
Project description:Chromatin modifying activities for construction of appropriate epigenetic landscapes by polycomb repressive complex 2 (PRC2) play an essential role in development and tumorigenesis. However, the spatiotemporal mechanisms by which PRC2 achieves diverse epigenomes for specific tissue or cellular contexts remain poorly understood. Here, we discovered that LATS2 knockout causes dysregulation of PRC2 and subsequent transcriptome changes for differentiation in both mouse and human cells. LATS2 depletion dependent dysregulation of PRC2 also effects H3K4me3 and forms negative feedback loop for maintenance of PRC2. Further analyses reveal that LATS2 on chromatin binds to EZH2 and LATS2 has ability to phosphorylate PRC2 in vitro. These LATS2 dependent H3K27me3 targets are highly induced during neurogenesis, and statistical analysis of glioblastoma multiforme reveals that LATS2-high cases show more dedifferentiated transcriptome and poor prognosis with silencing of H3K27me3 targets. These observations suggest that LATS2-mediated epigenome coordination is pivotal for development and disease, including cancer.
2016-07-26 | GSE63532 | GEO
Project description:Chromatin modifying activities for construction of appropriate epigenetic landscapes by polycomb repressive complex 2 (PRC2) play an essential role in development and tumorigenesis. However, the spatiotemporal mechanisms by which PRC2 achieves diverse epigenomes for specific tissue or cellular contexts remain poorly understood. Here, we discovered that LATS2 knockout causes dysregulation of PRC2 and subsequent transcriptome changes for differentiation in both mouse and human cells. LATS2 depletion dependent dysregulation of PRC2 also effects H3K4me3 and forms negative feedback loop for maintenance of PRC2. Further analyses reveal that LATS2 on chromatin binds to EZH2 and LATS2 has ability to phosphorylate PRC2 in vitro. These LATS2 dependent H3K27me3 targets are highly induced during neurogenesis, and statistical analysis of glioblastoma multiforme reveals that LATS2-high cases show more dedifferentiated transcriptome and poor prognosis with silencing of H3K27me3 targets. These observations suggest that LATS2-mediated epigenome coordination is pivotal for development and disease, including cancer. The rabeled cRNAs from Lats2-/- mouse embryonic fibroblasts (MEFs) and litter wild type MEFs were subjected to Agilent Mouse miRNA Microarray 8 x 15K. Each sample was run in biological dupulicate (different PDL).
2016-07-26 | E-GEOD-63532 | biostudies-arrayexpress
Project description:Background: Signaling by receptor tyrosine kinases (RTK) is frequently dysregulated in gliomas. Inter-individual variability in the causes for dysregulated RTK signaling may have hampered the efficacy of targeted therapies. Using gene expression modules around key regulators in the RAS-RAF-MEK-MAPK cascade and in the phosphatidylinositol 3-kinase-AKT pathways, we developed a âRMPAâ clustering scheme to distinguish gliomas with varying extents of RTK signaling. Results: We identified gene modules consistently co-expressed with NF1 (NF1-M), Sprouty (SPRY-M) and PTEN (PTEN-M) in gliomas. Their signatures enabled robust clustering of adult diffuse gliomas of WHO grades II-IV into RMPAhigh and RMPAlow phenotypes in a morphology-independent manner. In five independent data sets from three continents containing more than 1500 adult diffuse gliomas, RMPAhigh gliomas were associated with poor prognosis while RMPAlow gliomas were not. The RMPAhigh and RMPAlow glioma subtypes showed distinct levels of the activities of RAS-RAF-MEK-MAPK cascade and PI3K-AKT pathway and harbored unique sets of genomic alterations in the RTK signaling-related genes. The RMPAhigh gliomas contained large numbers of immature vessel cells and tumor associated macrophages and both cell types expressed high levels of pro-angiogenic RTKs including MET, VEGFR1, KDR, EPHB4 and NRP1. Conclusion: Inter-glioma variability in RTK signaling activities can be defined using the RMPA clustering scheme. The combined signatures of NF1-M, SPRY-M and PTEN-M reflect RTK signaling activity both in the glioma cells and in the glioma microenvironment. Our data show that RTK signaling in the glioma microenvironment may play a pivotal role in glioma progression. Transcriptome data from 22 fresh gliomas (2 astrocytoma II, 1 oligodendrocytoma II, 7 oligoastrocytoma II, 4 anaplastic oligoastrocytoma III and 8 GBM) were obtained using Affymetrix Human Gene 1.0 ST Array. Unsupervised hierarchical clustering of the expression data for the SPRY-M, NF1-M and PTEN-M was performed on these transcriptome data to identify samples with RMPAhigh or RMPAlow signature.
2015-10-30 | E-GEOD-74462 | biostudies-arrayexpress