Project description:DNA methylation analysis of 68 glioblastoma specimen of patients treated within clinical trials, 5 samples of normal brain tissue (non-tumor brain) and 4 tumor-derived glioma sphere lines. The data was used to identify changes in DNA methylation which contribute to the aberrant of expression of HOX transcription factors. Our group had previously demonstrated that expression of HOX genes was associated with increased resistance to chemo-radiotherapy and worse outcome in GBM patients Keywords: Disease state comparison Bisulphite converted genomic DNA from the 77 samples were hybridised to the Illumina Infinium 450 Human Methylation Beadchip
Project description:This SuperSeries is composed of the following subset Series: GSE24446: Genetic abnormalities in GBM brain tumors GSE24452: Genetic abnormalities in various cell subpopulations of GBM brain tumors GSE24557: Exon-level expression profiles of GBM brain tumors Refer to individual Series
Project description:DNA methylation analysis of 68 glioblastoma specimen of patients treated within clinical trials, 5 samples of normal brain tissue (non-tumor brain) and 4 tumor-derived glioma sphere lines. The data was used to identify changes in DNA methylation which contribute to the aberrant of expression of HOX transcription factors. Our group had previously demonstrated that expression of HOX genes was associated with increased resistance to chemo-radiotherapy and worse outcome in GBM patients Keywords: Disease state comparison
Project description:To investigate the transcriotome in glioblastoma tumor and normal brain on a single cell level, we performed RNA sequcening analysis with single cells derived from mouse normal brain tissue or GBM tumor tissue. Particularly, vascular endothelial cells (ECs) were traced using a Cdh5-Cre;LSL-tdTomato system.
Project description:Our main objective was to study genome-wide differential methylation in de novo glioblastoma multiforme (GBM, grade IV glioma). We evaluated CpG sites in gene promoters of 26,000+ genes using an array-based chip. We retrieved 54 GBM from biorepositories of two institutions(40 from Columbia University and 14 from Case Western Reserve University) and 24 control brain tissues from the New York Brain Bank, which collected control brain tissues from consented subjects without history of neurological diseases at autopsy. Bisulfite modified DNA was extracted from 54 GBM and 24 control brain tissue. The HumanMethylation27 Analysis Bead-Chips (Illumina) were used to interrogate 26,486 informative CpG sites in the autosomes.
Project description:Glioblastoma (GBM) is highly invasive primary brain tumor. Here, we retraced early steps of GBM invasion and interactions with tumor-associated myeloid cells (TAM) in a highly infiltrative murine GBM model in immunocompetent background. We reveal early mobilization of microglia in a wide onco-field ahead of GBM invasion, forming glial nets encircling tumor micro-infiltrates that are enmeshed with a dense network of extracellular matrix (ECM). Physical contacts with GBM cells initiate an astounding morphological, spatial, and functional transformation of microglia and monocyte-derived macrophages to form collectively organized migration streams with intertwined GBM cells, paralleled by major ECM restructuring along invasion tracks. Mechanistically, this requires upregulation of guidance receptor Plexin-B2 in TAM, which functions to resolve collisions with GBM cells by providing cell contact guidance for cell alignment and ECM restructuring. Together, our results on stage- and niche-specific mobilization of microglia/macrophages, on governing factors, and the molecular insights into pro-invasion signaling open new therapeutic opportunities to curb GBM invasion.
Project description:Glioblastoma (GBM) is highly invasive primary brain tumor. Here, we retraced early steps of GBM invasion and interactions with tumor-associated myeloid cells (TAM) in a highly infiltrative murine GBM model in immunocompetent background. We reveal early mobilization of microglia in a wide onco-field ahead of GBM invasion, forming glial nets encircling tumor micro-infiltrates that are enmeshed with a dense network of extracellular matrix (ECM). Physical contacts with GBM cells initiate an astounding morphological, spatial, and functional transformation of microglia and monocyte-derived macrophages to form collectively organized migration streams with intertwined GBM cells, paralleled by major ECM restructuring along invasion tracks. Mechanistically, this requires upregulation of guidance receptor Plexin-B2 in TAM, which functions to resolve collisions with GBM cells by providing cell contact guidance for cell alignment and ECM restructuring. Together, our results on stage- and niche-specific mobilization of microglia/macrophages, on governing factors, and the molecular insights into pro-invasion signaling open new therapeutic opportunities to curb GBM invasion.
Project description:Glioblastoma (GBM) is the most common and aggressive brain tumor in adults. The purpose of the present study was to identify GBM cell-selective secreted proteins by analyzing conditioned media (CM) from GBM, breast, and colon cancer cell lines using sequential window acquisition of all theoretical spectra mass spectrometry (SWATH-MS) and targeted proteomics. We identified 26,041 peptides derived from 2,371 proteins in the CM from GBM and the other cancer cell lines. Among the proteins identified, 15 showed significantly higher expression in the CM from GBM cell lines than in those from other cancer cell lines.
Project description:The recent incorporation of molecular features into the diagnosis of Glioblastoma Multiforme patients has led to an improved categorisation into different tumour subtypes with different prognosis and disease management. In this work, we have exploited the benefits of genome-wide multiomic approaches to identify potential molecular vulnerabilities existing on GBM patients. We used the Illumina MethylationEPIC Beadchip platform to describe the genome-wide 5mC and 5hmC DNA methylation landscape of a total of 9 patient-derived Glioblastoma Multiforme Cell lines obtained from the human glioblastoma cell culture resource (HGCC) and 4 brain samples obtained from non-tumoral controls