The differential expression of miRNA between murine glioma and PNET
Ontology highlight
ABSTRACT:
ORGANISM(S): synthetic construct Mus musculus
PROVIDER: GSE100065 | GEO | 2018/04/29
REPOSITORIES: GEO
Similar Datasets
Project description:Murine and human genome-wide microarray expression profiles (including GSE19404) were compared using Partek and Gene Set Enrichment Analysis (GSEA) in order to identify similarities. A murine PNET-like tumour by morphology was found to resemble human ATRT, whereas experimental glioma resembled a particular human glioblastoma subclass. Tumour material was resected or neurosphere cultures pelleted. Part of the material was processed for histological analysis, another was snap-frozen for isolation of RNA. RNA was then labelled and hybridised to Affymetrix MoEx-v1 arrays and analysed using Partek. This array dataset comprises Affymetrix MoEx-v2 microarrays hybridised with RNA from brain-derived tumour material (CA), subventricular zone (SVZ)-derived growth transformed neurospheres (CATR) and control neurospheres (CS, GFP).
2013-07-29 | E-GEOD-42515 | biostudies-arrayexpress
Project description:The lateral ventricle subventricular zone (SVZ) is a frequent and consequential site of pediatric and adult glioma spread, but the cellular and molecular mechanisms mediating this are poorly understood. We demonstrate that neural precursor cell (NPC):glioma cell communication underpins this propensity of glioma to colonize the SVZ through secretion of chemoattractant signals toward which glioma cells home. Biochemical, proteomic, and functional analyses of SVZ NPC-secreted factors revealed the neurite outgrowth-promoting factor pleiotrophin, along with required binding partners SPARC/SPARCL1 and HSP90B, as key mediators of this chemoattractant effect. Pleiotrophin expression is strongly enriched in the SVZ, and pleiotrophin knockdown starkly reduced glioma invasion of the SVZ in the murine brain. Pleiotrophin, in complex with the binding partners and signaling through the receptor PTPRZ1, activated glioma Rho/ROCK signaling, and ROCK inhibition decreased invasion toward SVZ NPC-secreted factors. These findings demonstrate a pathogenic role for NPC:glioma interactions and potential therapeutic targets to limit glioma invasion.
2017-07-26 | GSE99812 | GEO
Project description:Primary glioblastoma, representing over 90% of adult glioblastoma, develop rapidly without preexisting lower-grade glioma. We have generated a mouse model of primary glioblastoma driven by a single p53 mutation. These p53-mutant gliomas lose the syntenic region of human chromosome 10q, which is mapped to mouse chr19 and chr7. Loss of mouse chr19, containing Pten, activates PI3K/Akt signaling. Using serial MRI/3D-reconstruction, whole-genome sequencing and spectral karyotyping-based single-cell phylogenetic tree building, we showed two distinct types of tumor evolution in p53-mutant driven mouse models. Malignant gliomas/GBMs grew as a single mass (Type 1) and multifocal masses (Type 2), respectively, despite both exhibiting loss of Pten/chromosome 19 (chr19) and PI3K/Akt activation with sub-tetraploid/4N genomes. Analysis of early biopsied and multi-segment tumor tissues revealed no evidence of less proliferative diploid/2N lesions in Type 1 tumors. Strikingly, CA-derived relatively quiescent tumor precursors with ancestral diploid/2N genomes and normal Pten/chr19 were observed in the subventricular zone (SVZ), but was distantly segregated from multi-focal Type 2 tumors. Importantly, PI3K/Akt inhibition by Rictor/mTORC2 deletion blocked distant dispersal, restricting glioma growth in the SVZ.
2020-06-10 | GSE152071 | GEO
Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb and/or Pten. Rb and Pten deletion are important for prostate cancer progression. p53-/- Rbf/f vs p53-/- Rbâf/âf primary prostate cells. Three independent experiments were performed. p53-/- Rbf/f vs p53-/- Rbâf/âf Ptenâf/âf primary prostate cells. Four independent experiments were performed.
2015-12-31 | E-GEOD-68904 | biostudies-arrayexpress
Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb and/or Pten. Rb and Pten deletion are important for prostate cancer progression.
2015-12-31 | GSE68904 | GEO
Project description:As a starting point for dissecting the cellular heterogeneity of gliomas, different subpopulations from a CRISPR mouse model of glioma were profiled for gene expression. Because we initially identified these astrocyte subpopulations in the mouse brain, we first sought to determine whether their malignant analogues are present in mouse models of glioma. Towards this, we recently developed a mouse model of malignant glioma, one that utilizes E16.5 IUE approaches in combination with CRISPR mediated gene editing, where we use IUE to introduce gRNA vectors to delete NFI, PTEN, and p53, CAS9, and a GFP reporter, resulting in the generation of malignant glioma at P70. Using the GFP label to distinguish tumor from normal brain tissue, along with FACS-based selection against the glioma stem cell (GSC) and endothelial cells (see methods), we screened our tumor models for the presence of these prospective astroglial populations in the non-GSC fractions of these tumors.
2016-12-16 | GSE79437 | GEO
Project description:Primary glioblastoma, representing over 90% of adult glioblastoma, develop rapidly without preexisting lower-grade glioma. We have generated a mouse model of primary glioblastoma driven by a single p53 mutation. These p53-mutant gliomas lose the syntenic region of human chromosome 10q, which is mapped to mouse chr19 and chr7. Loss of mouse chr19, containing Pten, activates PI3K/Akt signaling. Rictor/mTORC2 deletion inhibits Akt signaling, causing a significant delay in p53-mutant driven glioma formation. Unexpectedly, Rictor/mTORC2 loss promotes p53-mutant driven medulloblastomas with unique features of pediatric SHH medulloblastoma. Mechanistically, Rictor/mTORC2 loss inhibits the generation of glioma precursor cells from neural stem/progenitor cells in the adult brain, while causing a delay in differentiation of granule cell precursors in the developing brain, a cell-of-origin of SHH medulloblastoma.
2018-06-01 | GSE78895 | GEO
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
Project description:Murine and human genome-wide microarray expression profiles (including GSE19404) were compared using Partek and Gene Set Enrichment Analysis (GSEA) in order to identify similarities. A murine PNET-like tumour by morphology was found to resemble human ATRT, whereas experimental glioma resembled a particular human glioblastoma subclass.
2013-07-29 | GSE42515 | GEO
Project description:Recently, we described a new animal model of CNS primitive neuroectodermal tumors (CNS-PNET), which was generated by orthotopic transplantation of human Radial Glial (RG) cells into NOD-SCID mice’s brain sub- ventricular zone. In the current study we conducted comprehensive RNA-Seq analyses to gain some insights on the mechanisms underlying tumorigenesis in this mouse model of CNS-PNET. Here we show that the RNA-Seq profiles derived from these tumors cluster with those reported for patients’ PNETs.
2017-06-12 | GSE82102 | GEO