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Project description:Reprogram glioblastoma (GBM) human cell line into DC
| PRJNA1128648 | ENA
Project description:Informed by the genetic alterations observed in human GBM, we engineered a novel, lentiviral injection mediated, mouse model of proneural GBM.
2017-07-12 | GSE99361 | GEO
Project description:Our laboratory has identified the Growth Hormone Receptor (GHR) as a candidate oncogenic pathway involved in GBM oncogenicity. In order to study further the role of GHR in GBM, we have generated GHR overexpressing patient-derived cell lines (PDCL) from PDCL established by GlioTEx team (Institut du Cerveau et de la Moelle, Paris, France). An analysis of the global proteome of each variant was then undertaken. The wild-type (GHR WT) and constitutively activated (GHR CA) GHR expression vectors were generous gifts from Mike Waters and Peter Brooks (University of Queensland, Australia). The constitutively activated GHR vector was generated by fusing the transmembrane and cytoplasmic domains of rabbit GHR (to ensure the absence of human GH stimulation) to Jun zippers in order to achieve GH-independent forced dimerization in absence of the extracellular domain. The control GFP vector was obtained from Addgene . These vectors were then inserted in lentiviral vectors. Cells were transduced with multiplicity of infection of 20 and transduced cells were selected with puromycin.
2022-06-23 | PXD004969 | Pride
Project description:Armatimonadetes bacterium DC isolate:DC Genome sequencing and assembly
| PRJNA285316 | ENA
Project description:The importance of extrinsic regulation of hematopoietic stem cell activity is increasingly acknowledged. Here we report the generation of a new niche system, which supports expansion of mouse hematopoietic stem cells in vitro. Characterization of this niche revealed a transcriptional regulatory network including four critical factors, namely FOS, SPI1, KLF10 and TFEC. Interestingly, these factors are essential for osteoclastogenesis, thus revealing an osteoclastic network that supports hematopoietic stem cell self-renewal. Lentiviral vectors containing putative transcription factors regulating HSC expansion were transfected into GPE cells and gene expression values were compared to empty vector controls.
2013-12-31 | E-GEOD-39835 | biostudies-arrayexpress
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: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:Single RNA-Seq on GBM cells from human GBM sample
| PRJNA820777 | ENA
Project description:Glioblastoma multiforme (GBM) is the most aggressive form of brain tumors. Despite radical surgery and radiotherapy supported by chemotherapy, the disease still remains incurable with extremely low median survival rate of 12-15 months from the time of initial diagnosis. The main cause of treatment failure is considered to be the presence of cells that are resistant to such treatment. MicroRNAs (miRNAs) as regulators of gene expression are involved in the tumor pathogenesis, including GBM. MiR-338 is a brain specific miRNA which has been described to target pathways involved in proliferation and differentiation. In our study, miR-338-3p and -5p were differentially expressed in GBM tissue in comparison to non-tumor brain tissue. Overexpression of miR-338-3p with miRNA mimic did not show any changes in proliferation rates in GBM cell lines (A172, T98G, U87MG). On the other hand, pre-miR-338-5p notably decreased proliferation and caused cell cycle arrest. Since radiation is currently the main treatment modality in GBM, we combined overexpression of pre-miR-338-5p with radiation, which led to significantly decreased of cell proliferation, and increased cell cycle arrest and apoptosis in comparison to only irradiated cells. To better elucidate the mechanism of action, we performed gene expression profiling analysis that revealed targets of miR-338-5p being Ndfip1, Rheb, ppp2R5a. These genes have been described to be involved in DNA damage response, proliferation and cell cycle regulation. To our knowledge, this is the first study to describe role of miR-338-5p in GBM and its potential to improve sensitivity of GBM to radiation. Study was performed on three glioblastoma multiforme cell lines A172, T98G and U87MG. This experiment was performed on Affymetrix GeneChip Human Gene ST 1.0 to elucidate the targets of miRNA-338-5p. Cell lines were seeded 24 hours prior transfection. After transfection with pre-miR338-5p or negative control cell were cultured for 24 hours and harvested. RNA was isolated using MirVana miRNA Isolation Kit (Ambion, USA) and checked for RNA integrity by Bioanalyzer 2100 and purity by ratios 260/280>1.8 and 260/230>1.8 by Nanodrop2000.
2015-12-10 | E-GEOD-75789 | biostudies-arrayexpress