Expression data of glioma samples from Henry Ford Hospital
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE4290 | GEO | 2006/04/10
SECONDARY ACCESSION(S): PRJNA94787
REPOSITORIES: GEO
Similar Datasets
Project description:mRNA expression data were collected from patients with brain tumor to improve diagnostic of gliomas on molecular level.
2007-06-24 | E-GEOD-4290 | biostudies-arrayexpress
Project description:The paper describes a model of glioma.
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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:Malignant gliomas represent the most devastating group of brain tumors in adults, among which glioblastoma multiforme (GBM) exhibits the highest malignancy rate. Despite combined modality treatment, GBM recurs and is invariably fatal. A further insight into molecular background of gliomagenesis is required to improve patient outcome. The first aim of this study was to gain broad information on miRNA expression pattern in malignant gliomas, mainly GBM. We investigated the global miRNA profile of malignant glioma tissues by means of miRNA microarrays, deep sequencing and meta-analysis. We selected miRNAs the most frequently deregulated in glioblastoma tissues as well as peritumoral brain areas in comparison to normal human brain. We found candidate miRNAs contributing to progression from gliomas grade III to gliomas grade IV. The meta-analysis of miRNA profiling studies in GBM tissues summarizes the past and recent advances in an investigation of miRNA signature in GBM versus noncancerous human brain and provides a comprehensive overview. We proposed a set of 35 miRNAs which expression is the most frequently deregulated in GBM patients and 30 miRNA candidates recognized as novel GBM biomarkers. miRNA expression profile in the adult malignant gliomas, glioma peritumoral tissues and normal human brain.
2014-09-26 | E-GEOD-61710 | biostudies-arrayexpress
Project description:Gliomas are aggressive lethal solid brain tumors arising from support cells in the central nervous system. Despite intense efforts to optimize the treatment of gliomas, the outcomes of high grade glioma patients are still frustrating. The causes and progress of gliomas have been investigated extensively; however, the genetic factors involved in the development of this disease remain poorly understood. We used microarrays to detail the global program of gene expression in different grade glioma tissues and try to find out some genes associated with the tumorigenesis of gliomas.
2013-04-10 | GSE45921 | GEO
Project description:Gliomas are aggressive lethal solid brain tumors arising from support cells in the central nervous system. Despite intense efforts to optimize the treatment of gliomas, the outcomes of high grade glioma patients are still frustrating. The causes and progress of gliomas have been investigated extensively; however, the genetic factors involved in the development of this disease remain poorly understood. We used microarrays to detail the global program of gene expression in different grade glioma tissues and try to find out some genes associated with the tumorigenesis of gliomas. Grade I to grade IV glioma tissues were selected in surgical operations for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain gene expression profiles. To that end, we hand-selected several genes that were differentially expressed in different grade glioma tissues and then performed a further study to identify the role of these genes in the process of the development of gliomas.
2013-04-10 | E-GEOD-45921 | biostudies-arrayexpress
Project description:Malignant gliomas represent the most devastating group of brain tumors in adults, among which glioblastoma multiforme (GBM) exhibits the highest malignancy rate. Despite combined modality treatment, GBM recurs and is invariably fatal. A further insight into molecular background of gliomagenesis is required to improve patient outcome. The first aim of this study was to gain broad information on miRNA expression pattern in malignant gliomas, mainly GBM. We investigated the global miRNA profile of malignant glioma tissues by means of miRNA microarrays, deep sequencing and meta-analysis. We selected miRNAs the most frequently deregulated in glioblastoma tissues as well as peritumoral brain areas in comparison to normal human brain. We found candidate miRNAs contributing to progression from gliomas grade III to gliomas grade IV. The meta-analysis of miRNA profiling studies in GBM tissues summarizes the past and recent advances in an investigation of miRNA signature in GBM versus noncancerous human brain and provides a comprehensive overview. We proposed a set of 35 miRNAs which expression is the most frequently deregulated in GBM patients and 30 miRNA candidates recognized as novel GBM biomarkers.
2014-09-26 | GSE61710 | 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 “RMPA” 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.
2015-10-30 | GSE74462 | 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:Analysis of the function of Tlx in regulating brain tumor stem cells (BTSCs) at the gene expression level. Based on our knowledge, we know that Tlx is specifically expressed in the neural stem cells in mouse brain. It also functionally regulates neurogenesis during the postnatal stages. The hypothesis tested in the present study is that Tlx influences the maintenance and progression of mouse brain gliomas through regulating the self-renewal of BTSCs and it is also a specific marker of brain tumor stem cells (BTSCs). Results provide important information about the function of Tlx in brain gliomas. Brain gliomas were initiated from the Nestin-CreERT2;Tlx flox/flox;Nestin-Tva transgenic mouse line. After 2.5 weeks, when the brain gliomas were fully developed, tamoxifen was administered through intraperitoneal injection. Tlx was knocked-out from the Cre-expressing littermates, but the littermates without Cre expression maintained intact Tlx function. Then, total RNA was obtained from mouse brain gliomas with severe neurological symptoms from the Tlx knockout and Tlx intact groups.
2013-04-17 | E-GEOD-46125 | biostudies-arrayexpress
Project description:Data includes all available Affymetrix SNP data from a cohort of Pediatric malignant glioma samples, isolated from Formalin-fixed Paraffin embedded tissue. No clinical data is available. Copy number analysis of Affymetrix 250K Sty SNP arrays was performed for 28 pediatric malignant gliomas. The VN algorithm was used to generate the reference signal based on 48 Mapping 500k HapMap Trio Dataset template.
2011-11-23 | E-GEOD-25589 | biostudies-arrayexpress