Ontology highlight
ABSTRACT:
PROVIDER: PRJNA679773 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13091500_1.fastq.gz | Fastqsanger.gz | |||
| SRR13091500_2.fastq.gz | Fastqsanger.gz | |||
| SRR13091501_1.fastq.gz | Fastqsanger.gz | |||
| SRR13091501_2.fastq.gz | Fastqsanger.gz | |||
| SRR13091502_1.fastq.gz | Fastqsanger.gz |
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Project description:Gliomas are aggressive lethal solid brain tumors arising from support cells in the central nervous system. Despite intense efforts to optimize the treatment of gliomas, the outcomes of high grade glioma patients are still frustrating. The causes and progress of gliomas have been investigated extensively; however, the genetic factors involved in the development of this disease remain poorly understood. We used microarrays to detail the global program of gene expression in different grade glioma tissues and try to find out some genes associated with the tumorigenesis of gliomas. Grade I to grade IV glioma tissues were selected in surgical operations for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain gene expression profiles. To that end, we hand-selected several genes that were differentially expressed in different grade glioma tissues and then performed a further study to identify the role of these genes in the process of the development of gliomas.
2013-04-10 | E-GEOD-45921 | biostudies-arrayexpress
Project description:Abstract:
Despite intensive treatments including temozolomide (TMZ) administration, glioblastoma patient prognosis remains dismal and innovative therapeutic strategies are urgently needed. A systems pharmacology approach was undertaken to investigate TMZ pharmacokinetics‐pharmacodynamics (PK‐PD) incorporating the effect of local pH, tumor spatial configuration and micro‐environment. A hybrid mathematical framework was designed coupling ordinary differential equations describing the intracellular reactions, with a spatial cellular automaton to individualize the cells. A differential drug impact on tumor and healthy cells at constant extracellular pH was computationally demonstrated as TMZ‐induced DNA damage was larger in tumor cells as compared to normal cells due to less acidic intracellular pH in cancer cells. Optimality of TMZ efficacy defined as maximum difference between damage in tumor and healthy cells was reached for extracellular pH between 6.8 and 7.5. Next, TMZ PK‐PD in a solid tumor was demonstrated to highly depend on its spatial configuration as spread cancer cells or fragmented tumors presented higher TMZ‐induced damage as compared to compact tumor spheroid. Simulations highlighted that smaller tumors were less acidic than bigger ones allowing for faster TMZ activation and their closer distance to blood capillaries allowed for better drug penetration. For model parameters corresponding to U87 glioma cells, inter‐cell variability in TMZ uptake play no role regarding the mean drug‐induced damage in the whole cell population whereas this quantity was increased by inter‐cell variability in TMZ efflux which was thus a disadvantage in terms of drug resistance. Overall, this study revealed pH as a new potential target to significantly improve TMZ antitumor efficacy.
Change the value of pH for different cases.
2019-09-30 | MODEL1909300003 | BioModels
Project description:Glioma study (gene expression and CGH): Brain tumours are the most common solid tumors in children and have the highest mortality rate of all solid pediatric tumours. Despite advances in multimodality therapy, children with high-grade gliomas invariably have an Overall Survival (OS) around 20% at 5 years. There is growing evidence that the biological knowledge and the histo-prognostic classifications used for the management of adult HGG may not fully apply to children. Interobserver variability and specificity of pediatric tumors with respect to the World Health Organization (WHO) classification have lead to a high rate of misclassification in multi-institutional studies. From 90 biopsies of children with HGG (High Grade Glioma), comprising 37 DIPG (Diffuse Infiltrating Pontine Glioma), 73 extracted RNA have been hybrized on Agilent 4x44K GE arrays and 71 extracted DNA have been hybrized on Agilent 44K and 4x44K CGH arrays. The dataset contains raw data files from Feature Extraction. Genomic data were jointly analysed with clinical and histological data comprising: date_of_diagnosis, date_of_last_news, WHO_grade, deceased_at_median_survival_time, deceased_at_2years, localization of the tumour in brain, gadolinium_T1_inf_T2. A specific analysis was performed on DIPG.
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Project description:We report a map of H3K4me3 - an activiting expression histone modification in C6 rat glioma cells. The data was obtained using whole genome high throughput technology. The sequencing was performed on Solid 5500xl platform. Examination of H3K4me3 histone modification in C6 rat glioma cell line
2015-05-07 | E-GEOD-46822 | biostudies-arrayexpress
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.
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Project description:This was a Phase II, open-label, non-randomized, multi-center study of oral dabrafenib in combination with oral trametinib in subjects with rare cancers harboring the BRAF V600E mutation including anaplastic thyroid cancer (ATC), biliary tract cancer (BTC), gastrointestinal stromal tumor (GIST), low grade (WHO G1/G2) glioma (LGG), high grade (WHO G3/G4) glioma (HGG), non-seminomatous germ cell tumors (NSGCT) / non-germinomatous germ cell tumors (NGGCT), adenocarcinoma of the small intestine (ASI), hairy cell leukemia (HCL) and multiple myeloma (MM).
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Project description:Gliomas are aggressive lethal solid brain tumors arising from support cells in the central nervous system. Despite intense efforts to optimize the treatment of gliomas, the outcomes of high grade glioma patients are still frustrating. The causes and progress of gliomas have been investigated extensively; however, the genetic factors involved in the development of this disease remain poorly understood. We used microarrays to detail the global program of gene expression in different grade glioma tissues and try to find out some genes associated with the tumorigenesis of gliomas.
2013-04-10 | GSE45921 | GEO
Project description:Several groups identified CSCs in solid tumors, including breast, brain, thyroid, melanoma, colon, pancreatic, liver, prostate, lung, head and neck, ovarian, and stomach cancers, by adopting many biomarkers. Here, we examined PRMS by gene expression microarray analysis for them. As a result, the tumor expressed various specific genes in each CSCs, SCs, FAPs, and PICs.
2022-05-25 | GSE203596 | GEO
Project description:Malignant gliomas are considered to be one of the deadliest human cancers, accounting for about 60% of all primary brain tumors. Cachexia is a complex metabolic derangement and muscle atrophy syndrome, which causes high mortalities in patients with advanced cancers including brain tumors. However, cachexia symptoms induced by gliomas and mechanisms underlying muscle atrophy are unclear. Herein, we developed a glioma cachexia model using nude mice orthotopicly implanted with two glioma cell lines (WHO II CHG5 and WHO IV U87). U87 mice developed more severe cachexia symptoms than CHG5 mice, including more evident anorexia, greater body weight loss and mortality. Unlike non-central nervous system cancer cachexia, glioma cachexia did not induce remarkable systemic inflammation but massive multi-organ atrophy. It also caused significantly decreased skeletal muscle mass and strength, which were associated with down-regulated myosin and AKT, and up-regulated AMPK, FOXO and Atrogin1. Interestingly, expressions of MuRF1, MyoD1, eIF3f, desmin and vimentin were not significantly changed. Consistently, NMR-based metabolomic analyses revealed pronounced metabolic derangements in cachectic gastrocnemius relative to controls. Glucose, glycerol, 3-hydroxybutyrate and glycine were remarkably down-regulated, whereas largely released amino acids due to proteolysis including glutamate, arginine, leucine and isoleucine were up-regulated in cachectic gastrocnemius. Moreover, glucose and lipid metabolism, protein biosynthesis and amino acid metabolism were disturbed dramatically in both glioma-bearing mice. U87 mice showed more changed metabolite levels and altered metabolic pathways. This work uncovers malignant grade-dependent glioma cachexia symptoms and metabolic derangements of skeletal muscle for the first time, and provides hints for new therapeutic approaches.
2018-09-22 | ST001064 | MetabolomicsWorkbench
Project description:We report a map of H3K4me3 - an activiting expression histone modification in C6 rat glioma cells. The data was obtained using whole genome high throughput technology. The sequencing was performed on Solid 5500xl platform.
2015-05-07 | GSE46822 | GEO