Similar Datasets
Project description:We profiled glioma samples to determine the histone modifications relative to different molecular markers, as well as different germline alterations.
2022-09-22 | GSE167804 | GEO
Project description:There is little overlap on publicily avaiable gene signatures and it is unclear how relevant these are to glioma biology. MYC is a very dynamically regulated gene, and it's gene signature will vary with respect to cell context. To determine what genes fall within the MYC signature of glioma, we performed ChIP-SEQ upon 4 different glioma PDX with two different MYC antibodies. The overlapping enriched genes will provide context of a MYC signature within the context of glioma.
2022-09-12 | GSE206873 | GEO
Project description:We used microarrays to determine the gene expression profile of different types of glioma Keywords: Disease state analysis
2008-09-09 | GSE12657 | GEO
Project description:<p>The UCSF Adult Glioma Study is a case-control study conducted at the University of California, San Francisco. The goals of the study were to discover inherited (genetic), developmental, immunologic and other risk factors for glioma and to determine molecular level tumor markers that would be helpful in classifying glioma into more homogeneous groups.</p>
| phs001497 | dbGaP
Project description:We used microarrays to determine the gene expression profile of different types of glioma Experiment Overall Design: Histologically identified glioma-subtypes were selected for RNA extraction and hybridization on Affymetrix microarrays (HG-U95A)
2008-10-25 | E-GEOD-12657 | biostudies-arrayexpress
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:The paper describes a model of glioma.
Created by COPASI 4.26 (Build 213)
This model is described in the article:
A mathematical model of pre-diagnostic glioma growth
Marc Sturrock, Wenrui Hao, Judith Schwartzbaum, Grzegorz A. Rempala
J Theor Biol. 2015 September 7; 380: 299–308
Abstract:
Due to their location, the malignant gliomas of the brain in humans are very difficult to treat in advanced stages. Blood-based biomarkers for glioma are needed for more accurate evaluation of treatment response as well as early diagnosis. However, biomarker research in primary brain tumors is challenging given their relative rarity and genetic diversity. It is further complicated by variations in the permeability of the blood brain barrier that affects the amount of marker released into the bloodstream. Inspired by recent temporal data indicating a possible decrease in serum glucose levels in patients with gliomas yet to be diagnosed, we present an ordinary differential equation model to capture early stage glioma growth. The model contains glioma-glucose-immune interactions and poses a potential mechanism by which this glucose drop can be explained. We present numerical simulations, parameter sensitivity analysis, linear stability analysis and a numerical experiment whereby we show how a dormant glioma can become malignant.
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2024-09-02 | BIOMD0000000801 | BioModels
Project description:The goal of this experiment was to compare the gene expression of glioma cells migrating on substrates of different topographies and to determine a migration-associated gene profile. Human malignant glioma U251MG cells were cultured on highly-aligned versus randomly-oriented electrospun nanofibers of poly-caprolactone. Cells migrated actively on aligned nanofibers but motility was very restricted on randomly-oriented fibers. Results of gene expression profiling indicated upregulation of a JAK/STAT signature in actively migrating glioma cells. Total RNA was extracted from 3 independent cultures of U251 glioma cells cultured on aligned versus random nanofibers and applied to Affymetrix HG-U133 plus 2 chips. Analysis of gene expression was used to determine a gene-signature correlated with different substrate topography
2011-03-24 | E-GEOD-28167 | biostudies-arrayexpress
Project description:Glioma initiating cells/stem cells exist in the bulk tumor of glioblastoma. This cell population contributes to the frequent resistances toward radiation/chemotherapy, aggressiveness of adult brain cancer and increased recurrence rate. Targeting stem cell population becomes one the most promising and permissive therapeutic strategies. We isolated glioma stem cells from patient-derived xenografts and profiled their epigenomic features, including 4 different DNA marks and 2 enhancer marks, and transcriptome in these in vitro cultured cell lines. Three fetal brain-derived neural stem/progenitors cells were used for comparing the unique and common molecular features in these glioma cancer stem cells.
2018-02-23 | GSE92460 | GEO
Project description:The role of brain immune compartments in glioma evolution remains elusive. We profiled immune cells in glioma microenvironment and the matched peripheral blood from 11 patients at a single-cell level. Notably, glioblastoma exhibits specific infiltration of certain blood-originated monocytes expressing EGFR ligands including EREG and AREG, coined as tumor-associated monocytes (TAMo). TAMo infiltration is mutually exclusive with EGFR alterations (P = 0.019), while co-occurring with mesenchymal subtype (P = 4.7x10-7) and marking worse prognosis (P = 0.004 and 0.032 in two independent cohorts). Evolutionary analysis of initial-recurrent glioma pairs and single-cell study of a multi-centric glioblastoma reveals remarkable association between elevated TAMo and glioma mesenchymal transformation. Further analysis identifies FOSL2 as a master regulator of TAMo. The roles of FOSL2-EREG/AREG-EGFR signaling axis in promoting glioma invasion were verified experimentally. Collectively, we have identified TAMo in tumor microenvironment and revealed its driving role in activating EGFR signaling to shape glioma evolution.
2023-08-01 | GSE237779 | GEO