Expression data from glioma patients
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: ryuya yamanaka
PROVIDER: E-GEOD-43378 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We used microarrays to select the genes associated glioma patients survival. This study aimed to define genes associated with survival. Expression profiling was performed on 50 gliomas. A gene classifier was developed.
2016-01-08 | GSE43378 | 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:HOX genes encode a family of homeodomain-containing transcription factors involved in the determination of cell fate and identity during embryonic development. They also behave as oncogenes in some malignancies. In this study, we found high expression of the HOXD9 gene transcript in glioma cell lines and human glioma tissues by quantitative real-time PCR. Using immunocytochemistry, we observed HOXD9 protein expression in human brain tumor tissues, including astrocytomas and glioblastomas. To investigate the role of HOXD9 in gliomas, we silenced its expression in the glioma cell line U87 using HOXD9-specific siRNA, and observed decreased cell proliferation, cell cycle arrest, and induction of apoptosis. It was suggested that HOXD9 contributes to both cell proliferation and/or cell survival. The HOXD9 gene was highly expressed in a side population (SP) of SK-MG-1 cells that was previously identified as an enriched-cell fraction of glioma cancer stem-like cells. HOXD9 siRNA treatment of SK-MG-1 SP cells resulted in reduced cell proliferation. Finally, we cultured human glioma cancer stem cells (GCSCs) from patient specimens found with high expression of HOXD9 in GCSCs compared with normal astrocyte cells and neural stem/progenitor cells (NSPCs). Our results suggest that HOXD9 may be a novel marker of GCSCs and cell proliferation and/or survival factor in gliomas and glioma cancer stem-like cells, and a potential therapeutic target. we analyzed the expression and function of HOXD9 in human gliomas and found high expression of HOXD9 in GCSCs. HOXD9 contributes to cell proliferation and/or survival in glioma cells and glioma cancer stem-like cells.
2011-04-16 | E-GEOD-28618 | biostudies-arrayexpress
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.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models .
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Please refer to CC0 Public Domain Dedication for more information.
2019-08-20 | BIOMD0000000801 | BioModels
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:Glioma initiating cells (GICs) are considered responsible for the therapeutic resistance and recurrence of malignant glioma. To clarify the molecular mechanism of GIC maintenance/differentiation, we established GIC clones from GBM patient tumors having the potential to differentiate into malignant gliomas in mouse intracranial xenograft, and established an in vitro glioma induction system by using serum stimulation. Upon the serum stimulation, the GIC spheres showed increased cellular proliferation, motility, filopodia/lameripodia formation and adhesion to the culture dishes. Simultaneously, the NSC marker proteins such as CD133 and Sox2 were down-regulated, and the astrocyte/glioma marker GFAP and the malignancy marker CD44 dramatically up-regulated. To identify genes/proteins whose expression changes dynamically during the differentiation of GICs into glioma cells, these GICs were subjected to DNA microarray/iTRAQ based integrated proteomics. Within 4 hours of tumor removal from GBM patients, tissues were subjected to GIC preparation. After successive cloning, total RNA from GIC clones (GIC03A and GIC03U) on day 2 or 7 of subculture in NSC medium with or without 10% FCS was subjected to the analysis with Affymetrix microarrays. Simultaneously, the proteins extracted from the same set of cells were subjected to LC-shot gun analyses using the 8-plex iTRAQ method. We sought to obtain the information of the common molecules that were up- or down-regulated during the GSC differentiation process, and functional targets for the early onset of GIC-associated glioma.
2013-01-26 | E-GEOD-43762 | biostudies-arrayexpress
Project description:Diffuse infiltrating gliomas are the most common primary brain malignancy found in adults, and Glioblastoma multiforme, the highest grade glioma, is associated with a median survival of 7 months. Transcriptional profiling has been applied to 85 gliomas from 74 patients to elucidate glioma biology, prognosticate survival, and define tumor sub-classes. These studies reveal that transcriptional profiling of gliomas is more accurate at predicting survival than traditional pathologic grading, and that gliomas characteristically express coordinately regulated genes of one of four molecular signatures: neurogenesis, synaptic transmission, mitotic, or extra-cellular matrix. Elucidation of these survival associated molecular signatures will aid in tumor prognostication and define targets for future directed therapy. Evaluate a large number of diffuse infiltrating gliomas through transcriptional profiling. Glioma tumor sub-classes may be identified through large scale gene expression studies. All patients undergoing surgical treatment at the University of California, Los Angeles for primary brain cancers between 1996 and 2003 were invited to participate in this Institutional Review Board approved study. 74 of the patients participating in this broad protocol were analyzed as part of this study if their initial tumor was diagnosed as a grade III (n=24) or IV (n=50) glioma of any histologic type on initial surgical treatment and fresh frozen material was obtained. Only grade III and IV gliomas were included in this study as the distinction between these grades is subtle and prone to misclassification. The time in days elapsed from resection to the day of death, or if the patient has remained alive, to the current day was recorded for all samples studied. Patient ages at diagnosis varied from 18 to 82 years. There were 46 females and 28 males. Probes were prepared using standard Affymetrix protocols, and hybridized to Affymetrix HG-U133A and HG-U133B arrays.
2007-12-20 | E-GEOD-4412 | biostudies-arrayexpress
Project description:This study aimed to define the genes associated with PCNSL patient survival. Expression profiling was performed on 34 PCNSLs. A gene classifier was developed. Thirty-four PCNSL patients were selected for RNA extraction and hybridization on Affymetrix microarrays.
2012-11-06 | E-GEOD-34771 | 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:Neural-tumor interactions drive glioma growth as evidenced in preclinical models, but clinical validation is limited. We present an epigenetically defined neural signature of glioblastoma that independently predicts patients’ survival. We use reference signatures of neural cells to deconvolve tumor DNA and classify samples into low- or high-neural tumors. High-neural glioblastomas exhibit hypomethylated CpG sites and upregulation of genes associated with synaptic integration. Single-cell transcriptomic analysis reveals a high abundance of stem cell-like malignant cells in high-neural glioblastoma, primarily of the neural lineage. These cells are further classified as neural precursor cell-like, astrocyte cell-like, and oligodendrocyte precursor-like, alongside oligodendrocytes and neurons. In line with these findings, high-neural glioblastoma cells engender neuron-to-glioma synapse formation in vitro and in vivo and show an unfavorable survival after xenografting. In patients, a high-neural signature associated with decreased survival. High-neural tumors also exhibit increased functional connectivity in magnetencephalography and resting-state magnet resonance imaging and can be detected via DNA analytes and brain-derived neurotrophic factor in patients’ plasma. The prognostic importance of the neural signature was further validated in patients diagnosed with diffuse midline glioma. Our study presents an epigenetically defined malignant neural signature in high-grade gliomas that is prognostically relevant. High-neural gliomas likely require a maximized surgical resection approach for improved outcomes.
2024-03-20 | GSE240704 | GEO