Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19545378_1.fastq.gz | Fastqsanger.gz | |||
| SRR19545378_2.fastq.gz | Fastqsanger.gz | |||
| SRR19545379_1.fastq.gz | Fastqsanger.gz | |||
| SRR19545379_2.fastq.gz | Fastqsanger.gz | |||
| SRR19545380_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Pediatric low-grade glioma incidence has been rising in the U.S., mirroring the rising rates of pediatric and maternal obesity. Recently, children of obese mothers were demonstrated to develop brain tumors at higher rates. Importantly, obesity in the U.S. is largely driven by diet, given the abudnance of high fat and high sugar food choices. We identified that combined maternal and postnatal obesogenic (Ob) diet exposure accelerated glioma formation in murine Neurofibromatosis type 1 (Nf1) optic pathway glioma (OPG)-forming mice, a model of pediatric glioma formation. Postnatal dietary exposure alone could not fully recaptiulate these effects, indicating maternal exposure was critical for this phenotype. To determine how Ob exposure affected gene expression in the optic nerve, we isolated Ob-exposed versus CD-exposed optic nerves and performed RNASeq. Enriched pathways included nervous system development, neuronal signaling and appetite regulation.
2025-05-27 | GSE269517 | GEO
Project description:The concept that solid tumors are maintained by a productive interplay between neoplastic and non-neoplastic elements has gained traction with the demonstration that stromal fibroblasts and immune system cells dictate cancer development and progression. While less studied, brain tumor (glioma) biology is likewise influenced by non-neoplastic immune system cells (macrophages and microglia) which interact with neoplastic glioma cells to create a unique physiological state (glioma ecosystem) distinct from that found in the normal tissue. To explore this neoplastic ground state, we leveraged several preclinical mouse models of neurofibromatosis type 1 (NF1) optic glioma, a low-grade astrocytoma whose formation and maintenance requires productive interactions between non-neoplastic and neoplastic cells, and employed whole tumor RNA-sequencing and mathematical deconvolution strategies to characterize this low-grade glioma ecosystem as an aggregate of cellular and acellular elements. Using this approach, we demonstrate that optic gliomas generated by altering the germline Nf1 gene mutation, the glioma cell of origin, or the presence of co-existing genetic alterations represent molecularly-distinct tumors. However, these optic glioma tumors share a 25-gene core signature, not found in normal optic nerve, that is normalized by microglia inhibition (minocycline), but not conventional (carboplatin) or molecularly-targeted (rapamycin) chemotherapy. Lastly, we identify a genetic signature conferred by Pten reduction and corrected by PI3K inhibition. This signature predicts progression-free survival in patients with either low-grade or high-grade glioma. Collectively, these findings support the concept that gliomas are composite ecological systems whose biology and response to therapy may be best defined by examining the tumor as a whole.
2017-08-07 | GSE102345 | GEO
Project description:Solid cancers develop within a supportive microenvironment that promotes tumor formation and continued growth through the elaboration of mitogens and chemokines. Within these tumors, monocytes (macrophages and microglia) represent rich sources of these stromal factors. Leveraging a genetically-engineered mouse model of neurofibromatosis type 1 (NF1) low-grade brain tumor (optic glioma), previous studies have demonstrated that microglia are important for glioma formation and maintenance. To identify the tumor-associated microglial factors that support glioma growth (gliomagens), we employed a comprehensive large scale discovery effort using optimized advanced RNA-sequencing methods. Candidate gliomagens were prioritized to identify potential secreted or membrane-bound proteins, which were next validated by quantitative RT-PCR and RNA FISH following minocycline-mediated microglial inactivation in vivo. Using these selection criteria, Ccl5 was identified as a highly expressed chemokine in both genetically engineered Nf1 mouse and human optic gliomas. As a candidate gliomagen, recombinant Ccl5 increased Nf1-deficient optic nerve astrocyte growth in vitro. Importantly, consistent with its critical role in maintaining tumor growth, Ccl5 inhibition with neutralizing antibodies reduced Nf1 mouse optic glioma growth in vivo. Collectively, these findings establish Ccl5 as critical stromal growth factor in low-grade glioma maintenance relevant to future microglia-targeted therapies for brain tumors.
2016-08-17 | GSE65831 | GEO
Project description:The study investigates the role of NF1 mutation and neuronal activity on the initiation of optic pathway glioma, a type of low-grade glioma. the RNAseq dataset investigates mRNA expression profile of human pilocytic astrocytomas (WHO grade I)
2021-03-30 | GSE163071 | GEO
Project description:Using a cytokeratin 5 gene promoter, we ectopically expressed a constitutively active zebrafish smoothened (smoa1) in presumably glial progenitor cells of zebrafish CNS. Stable transgenic zebrafish developed retinal tumors and low grade glioma of the optic nerve. Microarray analysis showed upregulation of Hh downstream targets of ptc1, gli1 and gli2a in tumors. Immunofluorescence studies confirmed overexpression of Pax2, GFAP, S100 and Sox2, specifically in gliomas. We also detected upregulated expression of phosphorylated pRb and Mdm2 associated with gliomagenesis. Our results suggest that dysregulated Hh signaling initiates tumorigenesis in zebrafish CNS. Zebrafish optic nerve maintains phosphorylated pRb expression, therefore provides a unique niche for pathogenesis of glioma. RNAs from 4 gross eye tumors (from fish of 4 months of age) and 4 normal eyes from wil-type control fish were extracted and used for array analysis
2013-09-07 | E-GEOD-40761 | biostudies-arrayexpress
Project description:Using a cytokeratin 5 gene promoter, we ectopically expressed a constitutively active zebrafish smoothened (smoa1) in presumably glial progenitor cells of zebrafish CNS. Stable transgenic zebrafish developed retinal tumors and low grade glioma of the optic nerve. Microarray analysis showed upregulation of Hh downstream targets of ptc1, gli1 and gli2a in tumors. Immunofluorescence studies confirmed overexpression of Pax2, GFAP, S100 and Sox2, specifically in gliomas. We also detected upregulated expression of phosphorylated pRb and Mdm2 associated with gliomagenesis. Our results suggest that dysregulated Hh signaling initiates tumorigenesis in zebrafish CNS. Zebrafish optic nerve maintains phosphorylated pRb expression, therefore provides a unique niche for pathogenesis of glioma.
2013-09-07 | GSE40761 | GEO
Project description:Changes in the gut microbiome can have profound effects on the nervous system through modulation of T cell and microglia function. Since our prior studies demonstrated that T cells and microglia positively regulate low-grade glioma growth through the establishment of T cell-microglia immune circuit, we sought to explore the impact of changes in the gut microbiota on tumor biology. For these studies, genetically engineered Neurofibromatosis type 1 (NF1) optic glioma (Nf1-OPG) mice were raised in a germ-free environment or treated with antibiotics to deplete gut bacteria. First, we demonstrated that Nf1-OPG mice raised in a germ-free (gnotobiotic) environment or treated with specific antibiotics lacked optic gliomas and had improved OPG-induced retinal pathology (increased retinal nerve fiber layer thickness). Second antibiotic-treated Nf1-OPG mice gavaged with fecal microbiota from Nf1-OPG mice raised in a standard barrier facility restored optic glioma growth. Third, we showed that both germ-free and antibiotic-treated Nf1-OPG mice exhibited reduced intra-tumoral CD8+ T cell content resulting from decreased microglia chemokine production. Collectively, these findings establish a mechanistic relationship between the gut microbiota and brain tumor growth relevant to potential therapeutic interventions for pediatric low-grade gliomas.
2025-03-05 | GSE270264 | GEO
Project description:NF1 mutation drives neuronal activity-dependent optic glioma initiation
| PRJNA684596 | ENA
Project description:Gioma stem cells from Nf1-associated optic gliomas and NSCs from third ventricle zone show differencies in gene expression patterns and physiological functions. We used microarrays to identify differential gene expression between glioma stem cells and the control counterparts including the wild type and Nf1-/- neural stem cells from the third ventricle.
2014-12-01 | GSE58260 | GEO
Project description:Dissecting systemic risk factors for NF1 optic glioma formation and growth in mice.
| PRJNA701259 | ENA