Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA130589 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We compared a large panel of human glioblastoma stem-like (GS) cell lines, corresponding primary tumors and conventional glioma cell lines to identify cell lines that preserve the transcriptome of human glioblastomas most closely, thereby allowing identification of shared therapeutic targets. We used Affymetrix HG-U133 Plus 2.0 microarrays to compare human glioblastoma stem-like (GS) cell lines, corresponding primary tumors and conventional glioma cell lines. We extracted total RNA from 32 conventional glioma cell lines, 12 GS cell lines (8 in two different passages), 7 clonal sublines derived from two GS lines, 12 original tumors, and 4 monolayer cultures established from the same tumors as GS-lines using standard serum conditions.
2011-02-12 | E-GEOD-23806 | biostudies-arrayexpress
Project description:We compared a large panel of human glioblastoma stem-like (GS) cell lines, corresponding primary tumors and conventional glioma cell lines to identify cell lines that preserve the transcriptome of human glioblastomas most closely, thereby allowing identification of shared therapeutic targets. We used Affymetrix HG-U133 Plus 2.0 microarrays to compare human glioblastoma stem-like (GS) cell lines, corresponding primary tumors and conventional glioma cell lines.
2011-02-12 | GSE23806 | GEO
Project description:<p>We used massively parallel, paired-end sequencing of expressed transcripts (RNA-seq) to detect novel gene fusions in short-term cultures of glioma stem-like cells freshly isolated from nine patients carrying primary glioblastoma multiforme (GBM). The culture of primary GBM tumors under serum-free conditions selects cells that retain phenotypes and genotypes closely mirroring primary tumor profiles as compared to serum-cultured glioma cell lines that have largely lost their developmental identities.</p>
| phs000505 | dbGaP
Project description:Glioblastoma represents the most common and aggressive primary brain tumor type in adults. Stem cell regulatory pathways have been shown to be activated in gliomas supporting self-renewal, tumor maintenance and survival under stress. Glioblastoma stem-like phenotype, cell motility and tumor cell heterogeneity are considered significant hurdles to overcome for developing new treatment against these tumors. Transcription factor PROX1 has been associated with stem-like-phenotypes. Here, we overexpressed and suppressed PROX1 in glioma cell lines in order understand the gene expression regulated by this transcription factor.
2018-12-29 | E-MTAB-6991 | biostudies-arrayexpress
Project description:Glioblastomas are the most lethal tumors affecting the central nervous system in adults. Simple and inexpensive syngeneic in vivo models that closely mirror human glioblastoma, including interactions between tumor and immune cells, are urgently needed for deciphering glioma biology and developing more effective treatments. Here, we generated mouse glioblastoma cell lines by repeated in-vivo passaging of neural stem cells and tumor tissue of a neural stem cell-specific Pten/p53 double-knockout genetic mouse model. Transcriptome and genome analyses of the cell lines revealed molecular heterogeneity comparable to that observed in human glioblastoma. Upon orthotopic transplantation into syngeneic hosts they formed high-grade gliomas that faithfully recapitulated the histopathological characteristics, invasiveness and infiltration by myeloid cells characteristic of human glioblastoma. These features make our cell lines unique and useful tools to study multiple aspects of glioma pathomechanism and test immunotherapies in syngeneic preclinical models.
2021-01-27 | GSE145558 | GEO
Project description:Glioblastomas are the most lethal tumors affecting the central nervous system in adults. Simple and inexpensive syngeneic in vivo models that closely mirror human glioblastoma, including interactions between tumor and immune cells, are urgently needed for deciphering glioma biology and developing more effective treatments. Here, we generated mouse glioblastoma cell lines by repeated in-vivo passaging of neural stem cells and tumor tissue of a neural stem cell-specific Pten/p53 double-knockout genetic mouse model. Transcriptome and genome analyses of the cell lines revealed molecular heterogeneity comparable to that observed in human glioblastoma. Upon orthotopic transplantation into syngeneic hosts they formed high-grade gliomas that faithfully recapitulated the histopathological characteristics, invasiveness and infiltration by myeloid cells characteristic of human glioblastoma. These features make our cell lines unique and useful tools to study multiple aspects of glioma pathomechanism and test immunotherapies in syngeneic preclinical models.
2021-01-27 | GSE145557 | GEO
Project description:The DNA methylation profiles of Glioma Stem Cell (GSC) lines were investigated in order to find the stem cell signature associated to glioblastoma (GBM). This goal was achieved through the comparison of GSC methylation data with FFPE-GBM biopsies and human foetal Neural Stem Cell (NSC) lines profiles.
2013-03-08 | GSE41824 | GEO
Project description:Recent studies demonstrated that tumor cells with stem cell-like properties can be cultured from human glioblastomas by using conditions that select for the expansion of neural stem cells. We established glioblastoma stem-like (GS-) cell cultures from 9 different glioblastomas, 8 of which generated stably expandable cell lines. Analyzing GS-cell cultures, we discovered two clearly discernable phenotypes. Microarray analysis showed that the 4 GSf cell lines shared expression profiles dominated by genes involved in nervous system development and neuropeptide signaling, while the 5 GSr lines shared expression signatures enriched for extracellular matrix-proteins. Keywords: Cell line comparison
2007-12-04 | GSE8049 | GEO
Project description:Glioblastoma is one of the deadliest malignancies worldwide and is virtually incurable due to its highly infiltrative growth and limited sensitivity to conventional treatment by radiochemotherapy. It is hypothesized that a small population of cells with a stem-like phenotype is the major culprit of tumor recurrence. These cells are characterized by an enhanced DNA repair capacity and expression of stemness marker genes, and elimination of this population might delay or even stop tumor recurrence following radiochemotherapy. The aim of this study was to analyze whether interference with the Hedgehog signaling (Hh) pathway or combined Hh/Notch blockade can efficiently target these cancer stem cells and sensitize them to chemotherapeutic drugs. Using tumor sphere lines and primary glioma cells we demonstrate that the Hh pathway inhibitor GANT61 (GANT) and the Hh/Notch inhibitor arsenic trioxide (ATO) are capable to synergistically decrease proliferation and induce cell death in combination with the natural cotton derived anticancer agent (-)-Gossypol (Gos). In contrast to GANT in combination with Gos, the ATO/Gos combination also strongly prevented sphere formation and recovery. These synergistic effects were associated with major proteomic changes indicating decreased cell movement, distortion of cell cycle and DNA repair, as well as markedly reduced stemness. Collectively, our data show that ATO and Gos, two drugs that are safe for use in humans, represent a promising targeted therapy approach for the synergistic and specific elimination of glioma stem-like cells.
2019-03-13 | PXD009249 | Pride
Project description:Cancer-specific coding mutations can create neoantigens that can be presented on the cell surface of tumors to trigger immunogenic clearance1–4. However, current cancer vaccine approaches have not been universally effective5; this is especially true in tumors with a low mutational burden which, in turn, carry a low conventional neoantigen load6. Transposable elements (TEs) make up approximately 50% of the human genome and have been discovered to provide cryptic promoters, which can be reactivated with epigenetic manipulations to generate TE-gene chimeric transcripts that can be translated into noncanonical peptides7. Here, we focus on glioblastoma, an aggressive brain cancer with low mutation burden, to explore whether epigenetic therapy can induce TE-chimeric antigens (TEAs) to appreciably increase the antigen repertoire that can be targeted with immunotherapy. We perform comprehensive epigenetic and transcriptomic profiling of three patient-derived glioblastoma stem cell lines (GSCs) and, more importantly, astrocyte and fibroblast primary cell lines that are either proliferating or quiescent, treated with epigenetic therapy drugs to identify treatment-induced TEA (TI-TEA) candidates that are preferentially expressed in cancer cells. Although we verify TI-TEAs are indeed presented on HLA molecules in GSCs thus are promising cancer vaccine candidates, many TEs were also transcriptionally activated in proliferating primary cell lines after epigenetic therapy. This work presents a cautionary but optimistic tale for future efforts in harnessing TI-TEAs for targeted immunotherapy approaches.
2024-06-05 | PXD039893 | Pride