Single-cell RNA sequencing analysis of mouse normal brain and GBM tumors
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA819475 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18473455.fastq.gz | Fastqsanger.gz | |||
| SRR18473456.fastq.gz | Fastqsanger.gz | |||
| SRR18473457.fastq.gz | Fastqsanger.gz | |||
| SRR18473458.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
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
2010-11-21 | E-GEOD-24558 | biostudies-arrayexpress
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.
2023-02-17 | GSE199379 | GEO
Project description:The characteristics of immune cells infiltrating pediatric brain tumors is largely unexplored. A better understanding of these characteristics will provide a foundation for development of immunotherapy for pediatric brain tumors. Gene expression profiles were used to identify immune marker gene that are differentially expressed between various brain tumor types. Gene expression profiles were generated from surgical tumor and normal brain samples (n=130) using Affymetrix HG-U133plus2 chips (Platform GPL570). Gene expression profiles of different types of brain tumors and normal brain were filtered to obtain gene expression of key immune cell markers. Comparative analyses between different brain tumors and normal brain was used to identifiy differential immune characteristics of these tumors.
2013-08-25 | E-GEOD-50161 | biostudies-arrayexpress
Project description:GBM is a heterogenous tumor. Based on membrane protein expression, the GBM single cell dissociates were seperated into different subfractions by FACS assay. The genomic aberration among each populations were compared by analysis of CGH data. Genomic DNA were extracted from sorted cell population and CGH assay were performed to compare the similarity genomic abnormality among different cell groups.
2010-11-21 | E-GEOD-24452 | biostudies-arrayexpress
Project description:Human Glioblastoma Multiforme tumors taken before dendritic cell vaccination, the recurrent tumors taken after vaccination and control GBM tumors from non vaccinated patients. Experiment Overall Design: Six Glioblastoma Multiforme patients underwent surgery. Their brain tumors were removed and analyzed via microarray. The lysate from the tumors were cultured with the patients' dendritic cells and the DCs were injected back into the patients. The patients GBMs returned and they underwent surgery a second time and those tumors were also analyzed via microarray. Tumors from the first and second GBM surgeries of 5 patients who did not receive DC vaccines are included as controls.
2009-04-11 | E-GEOD-11100 | biostudies-arrayexpress
Project description:Examine the genetic abnormality in brain tumors Genomic DNA were extracted from frozen brain tumor samples and CGH assay were performed to compare the similarity genomic abnormality among different cell groups.
2010-11-21 | E-GEOD-24446 | biostudies-arrayexpress
Project description:We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18INK4C and p16INK4A codeletion. Functional reconstitution of p18INK4C in GBM cells null for both p16INK4A and p18INK4C resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18INK4C in p16INK4A-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16INK4A in primary astrocytes induced a concomitant increase in p18INK4C. Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18INK4C in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation. Keywords: comparative genomic hybridization DNA copy number abberation of human glioblastoma tumors were obtained by comparative genomic hybridization of GBM tumor vs. normal human DNA. 11 human GBM samples were analyzed on Agilent human 244A human cgh array (G4411B). Normal Human DNA was used as reference. Some samples were hybridized with dye-swap replica.
2008-04-29 | E-GEOD-9177 | biostudies-arrayexpress
Project description:Glioblastoma (GBM) is the most common and aggressive primary brain malignancy. Adhesion G protein-coupled receptors (aGPCRs) have attracted interest for their functional role in gliomagenesis and their potential as treatment targets. To identify therapeutically targetable opportunities among aGPCR family members in an unbiased fashion, we analyzed expression levels of all aGPCRs in GBM and non-neoplastic brain tissue. Using bulk and single cell transcriptomic and proteomic data, we show that CD97 (ADGRE5), an aGPCR previously implicated in GBM pathogenesis, is the most promising aGPCR target in GBM, by virtue of its abundance in all GBM tumors and its de novo expression profile in GBM compared to normal brain tissue and neural progenitors. CD97 knockdown or knockout significantly reduces the tumor initiation capacity of patient-derived GBM cells (PDGC) in vitro and in vivo. Transcriptomic and metabolomic data from PDGCs suggest that CD97 promotes glycolytic metabolism. The oncogenic and metabolic effects of CD97 are mediated by the MAPK pathway. Activation of MAPK signaling depends on phosphorylation of the cytosolic C-terminus of CD97 and recruitment of -arrestin. Using single-cell RNA-sequencing and biochemical assays, we demonstrate that THY1/CD90 is the most likely CD97 ligand in GBM. Lastly, we show that targeting of GBM cells with an anti-CD97 antibody-drug conjugate in vitro selectively kills tumor cells but not human astrocytes or neural stem cells. Our studies identify CD97 as an important regulator of tumor metabolism in GBM, elucidate mechanisms of receptor activation and signaling, and provide strong scientific rationale for developing biologics to target CD97 in GBM.
2023-12-01 | GSE230389 | GEO
Project description:Glioblastoma multiforme (GBM) is the most common form of malignant glioma and is characterized by marked genetic instability, extensive intra-tumoral histopathological variability, and unpredictable variation in its clinical behavior. We investigated global gene expression in surgical samples of primary brain tumors. Gene expression profiling revealed large differences between normal brain samples and tumor tissues and between GBMs and lower grade oligodendroglial tumors. Extensive differences in gene expression were found among GBMs, particularly in genes involved in angiogenesis, immune cell infiltration, and extracellular matrix re-modeling. Significantly, we found that the global gene expression patterns in paired specimens from the same GBM invariably were more closely related to each other than to any other tumor, even when the paired specimens had strikingly divergent histologies. Survival analyses revealed a set of approximately 70 genes that were more highly expressed in rapidly progressing tumors and which stratified GBMs into two groups that differed by more than four-fold in median duration of survival. We further investigated one gene from the group, FABP7, and confirmed its association with survival in two unrelated cohorts totaling 105 patients. Expression of FABP7 enhanced the motility of glioma-derived cells in vitro. Our analyses thus provide a series of prognostic markers and suggest that their expression may enhance the invasive potential of tumor cells.
2005-11-11 | E-SMDB-2677 | biostudies-arrayexpress