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GBM cell lines derived and propagated according to Cambridge protocol

ABSTRACT: We screened the gene expression in GBM cell lines cultured under serum-free conditions. We have special interest in genes associated with glial development such as NG2, Olig2 and PDGFRa. This microarray data gave us an idea about the expression of these genes and made the basis for further investigation. Seven GBM cells were derived from 7 different patients under serum-free conditions according to Cambridge protocol as previously described (Fael Al-Mayhani et al, 2009). The RNA was extracted and its quality was assessed. The samples were sent for microarray screening using Illumina platform. The gene was considered as present when the detection value was greater than 0.99.

ORGANISM(S): Homo sapiens

SUBMITTER: Colin Watts

PROVIDER: E-GEOD-15846 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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GBM cell lines derived and propagated according to Cambridge protocol

Project description:We screened the gene expression in GBM cell lines cultured under serum-free conditions. We have special interest in genes associated with glial development such as NG2, Olig2 and PDGFRa. This microarray data gave us an idea about the expression of these genes and made the basis for further investigation.

2009-04-28 | GSE15846 | GEO

Glioblastoma serum biomarkers identification by iTRAQ

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2019-03-04 | PXD012207 | Pride

Epigenetic determinants of self-renewal in glioblastoma

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2015-11-11 | E-GEOD-63296 | biostudies-arrayexpress

Epigenetic determinants of self-renewal in glioblastoma

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Transcription profiling by array of human Glioblastoma multiforme (GBM) tumor samples to asses the intra-tumoral heterogeneity at the gene expression level

Project description:Glioblastoma multiforme (GBM) is a highly heterogeneous disease that shows an enourmous range of genetic abnormalities in comparison to other astrocytic tumors. Intra-patient heterogeneity in GBM has been poorly characterized both at phenotypic and genomic level. During surgical GBM resections, we have extracted between 4 and 8 tumor subsamples from different areas of the malignant tissue that were at least 1cm apart. Our aim to asses the intra-tumoral heterogeneity at the gene expression level to uncover important dynamics underlying GBM progression that may have relevant implication for treatment.

2013-02-16 | E-MTAB-1129 | biostudies-arrayexpress

Profiling by array of human Glioblastoma multiforme (GBM) tumor samples to asses the intra-tumoral heterogeneity in genomic copy number aberrations

Project description:Glioblastoma multiforme (GBM) is a highly heterogeneous disease that shows an wide range of genetic abnormalities in comparison to other astrocytic tumors. We have extracted between 4 and 8 tumor subsamples from different areas of the malignant tissue that were at least 1cm apart. Our aim to asses the intra-tumoral heterogeneity by comparing copy number aberrations in different tumor areas to uncover important dynamics underlying GBM progression.

2013-02-15 | E-MTAB-1215 | biostudies-arrayexpress

NAC, Tiron and Trolox impair GBM tumorigenic cell survival by mechanisms independent from antioxidant activity

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Glioma stem cell treatment with MELK-signaling inhibitors

Project description:Glioblastoma multiforme (GBM) is a highly lethal brain tumor. Due to resistance to current therapies, patient prognosis remains poor and development of novel and effective GBM therapy is crucial. Glioma stem cells (GSCs) have gained attention as therapeutic target in GBM due to their relative resistance to current therapies and potent tumor-initiating ability. Recent studies including our own identified that the mitotic kinase, maternal embryonic leucine-zipper kinase (MELK), is highly expressed in GBM tissues, specifically in GSCs, and its expression is inversely correlated with the post-surgical survival period of GBM patients. In addition, patient-derived GSCs depend on MELK for their survival and growth both in vitro and in vivo. Here, we provide evidence that the kinase activity of MELK is essential for the action of MELK in GSCs and vital for GBM growth. We utilized in silico structure-based analysis for protein-compound interaction to predict that a recently identified small molecule, Compound 1 (C1), binds to the kinase-active site of MELK protein and eliminates MELK kinase activity in nanomolar concentrations. When treated with C1, GSCs undergo mitotic arrest and subsequent cellular apoptosis in vitro, a phenotype identical to that observed using MELK shRNA-mediated knockdown. C1 treatment strongly induces tumor cell apoptosis in slice cultures of GBM surgical specimens and attenuates growth of mouse intracranial tumors derived from GSCs in a dose-dependent manner. Lastly, C1 treatment sensitizes GSCs to radiation treatment. Collectively, these data indicate that targeting MELK kinase activity is a promising approach to attenuate GBM growth by eliminating GSCs in tumors. Microarray-based expression analysis of glioma stem cells treated with MELK-signaling inhibitors

2013-08-28 | E-GEOD-50227 | biostudies-arrayexpress

SEVERE CONSEQUENCES OF A HIGH-LIPID DIET INCLUDE HYDROGEN SULFIDE DYSFUNCTION AND DISEASE AGGRESSION IN GLIOBLASTOMA

Project description:Glioblastoma (GBM) remains among the deadliest of human malignancies, and the emergence of the cancer stem cell (CSC) phenotype represents a major challenge to durable treatment response. Because the environmental and lifestyle factors that impact CSC populations are not clear, we sought to understand the consequences of diet on CSC enrichment. We evaluated disease progression in mice fed an obesity-inducing high-fat diet (HFD) versus a low-fat, control diet. HFD resulted in hyper-aggressive disease accompanied by CSC enrichment and shortened survival. HFD drove intracerebral accumulation of saturated fats, which inhibited the production of the cysteine metabolite and gasotransmitter, hydrogen sulfide (H2S). H2S functions principally through protein S-sulfhydration and regulates multiple programs including bioenergetics and metabolism. Inhibition of H2S increased proliferation and chemotherapy resistance, whereas treatment with H2S donors led to death of cultured GBM cells and stasis of GBM tumors in vivo. GBM specimens present an overall reduction in protein S-sulfhydration, primarily associated with proteins regulating cellular metabolism. These findings provide new evidence that diet modifiable H2S signaling serves to suppress GBM by restricting metabolic fitness, while its loss triggers CSC enrichment and disease acceleration. Interventions augmenting H2S bioavailability concurrent with GBM standard of care may improve outcomes for GBM patients.

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