Expression data from mice brain implanted GSC272 glioma stem cells or POSTN knockout
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Soon Young Park
PROVIDER: E-GEOD-73071 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Differential mRNA expression patterns were seen in GSC272-vector compared to GSC272-POSTN shRNA tumors. We used microarrays to POSTN regulated gene expression in glioma stem cells.
2015-09-16 | GSE73071 | GEO
Project description:Expression data from mice brain implanted GSC272 glioma stem cells or POSTN knockout
| PRJNA295982 | ENA
Project description:Glioblastoma multiforme (GBM) brain tumours have one of the shortest mean survival times (<1 year). In vivo models of GBM in mice and rats have been developed to study aspects of glioma that cannot be observed in cell culture such as angiogenesis, invasion and metastasis. Gliomas can be induced by implantation of rodent glioma cell lines into the brain or flank of nude mice. The disadvantages of rodent models however include variable growth rate and poor penetrance, which leads to difficulties in collecting clearly graded samples (pre-vascular/vascular). Bikfalvi et al have previously established a human GBM model that addresses these issues based on the chicken egg chorio-allantoic membrane (CAM), a highly vascularised extra-embryonic tissue. We have used DNA microarrays and a CAM model of GBM to study gene expression during the recruitment and development of the tumour vasculature. Over a 5 day period samples were taken every 12 hours from the tumour implantation site consisting of tumour cells and stroma cells, and also from a site distant from the implantation site consisting of just CAM cells. This study will shed light on the dynamic transcriptional signature of pathological angiogenesis. On day 10 of embryonic development 3-5 million U87 cells were deposited onto the surface of the CAM after gentle laceration. The cells were contained within a plastic ring and each tumour was size matched based on its volume. Tumour/stroma and distant CAM samples were cut out at 12 hour intervals post implantation for 5 days, equalling 10 time points. Each time point consisted of three replicates. U87 cells in culture (pre-implantation) were also included in the study in triplicate.
2013-12-02 | E-GEOD-43674 | biostudies-arrayexpress
Project description:Glioblastoma multiforme (GBM) brain tumours have one of the shortest mean survival times (<1 year). In vivo models of GBM in mice and rats have been developed to study aspects of glioma that cannot be observed in cell culture such as angiogenesis, invasion and metastasis. Gliomas can be induced by implantation of rodent glioma cell lines into the brain or flank of nude mice. The disadvantages of rodent models however include variable growth rate and poor penetrance, which leads to difficulties in collecting clearly graded samples (pre-vascular/vascular). Bikfalvi et al have previously established a human GBM model that addresses these issues based on the chicken egg chorio-allantoic membrane (CAM), a highly vascularised extra-embryonic tissue. We have used DNA microarrays and a CAM model of GBM to study gene expression during the recruitment and development of the tumour vasculature. Over a 5 day period samples were taken every 12 hours from the tumour implantation site consisting of tumour cells and stroma cells, and also from a site distant from the implantation site consisting of just CAM cells. This study will shed light on the dynamic transcriptional signature of pathological angiogenesis.
2013-12-02 | GSE43674 | GEO
Project description:Albeit vascular prostheses for the replacement of large arteries (e.g. aorta) are commercially available for decades, small-diameter vascular grafts (e.g., for coronary artery bypass graft surgery) still remain an unmet clinical need. Biostable polymers commonly used for the fabrication of aortic prostheses (e.g., poly(ethylene terephthalate) or expanded poly(tetrafluoroethylene)) have insufficient haemocompatibility to withstand thrombosis at low blood flow characteristic of small arteries (e.g., coronary artery). Hence, researchers endeavor to develop a biodegradable, tissue-engineered vascular graft (TEVG) to avoid the use of autologous blood vessels, such as saphenous vein or internal mammary artery, as conduits during the bypass surgery. Although a number of promising prototypes have been designed to date, none of them passed the pre-clinical trials successfully. Implantation into the ovine or porcine arteries is associated with thrombosis, neointimal hyperplasia, and aneurysms within one-year postoperation, precluding further clinical translation of TEVGs. Among the reasons of such impediment is that pathophysiology of TEVG implantation remains unclear and the molecular events occurring in the TEVG upon its implantation have not been properly investigated hitherto. Here, we for the first time performed a proteomic profiling of the TEVGs (n = 12) implanted into the ovine carotid arteries for one year and suffered from thrombosis to identify the signatures of TEVG failure in an unbiased manner. Contralateral intact ovine carotid arteries (n = 12) have been selected as a control group.
2022-11-26 | PXD036520 | Pride
Project description:Knowledge of genes expression related to the growth-inhibition biological effects induced by low-energy N+ in plant. This study investigated the differentially expressed genes (DEGs) related to the growth-inhibition biological effects induced by low-energy N+ in plant by RNA-seq. Ion fluences (40Kev, curren intensity=3mA) of 1×1017N+/cm2，2×1017N+/cm2，4×1017N+/cm2，6×1017N+/cm2，8×1017N+/cm2 were used in the ion-implanted experiments. Biological effects with growht-inhibition were arised from the samples implanted by the ion fluences of 6×1017N+/cm2，8×1017N+/cm2 because of the inhibition of seedling height and root length. We sequenced mRNA from these damaged rice seedlings and others. We identified 776 transcripts as reliable DEGs at the growth inhibition sample campared with the control.The pathway enrichment analysis of these 776 DEGs showed that pathway of photosynthesis - antenna proteins was down-regulated. Meanwhile transcription factor analysis showed that genes related to AUX/IAA were also down-regulated. This study were contributed to a better understanding of molecular events responsible for adaption to the implantation of low-energy ion beam in plant.
2016-04-09 | GSE45908 | GEO
Project description:Cyclophosphamide (CPA) treatment on a six-day repeating metronomic schedule induces a dramatic, innate immune cell-dependent regression of implanted gliomas. However, little is known about the underlying mechanisms of innate immune cell mobilization and recruitment, or about the role of DNA damage and cell stress response pathways in eliciting the anti-tumor immune responses linked to tumor regression. To address these questions, we compared untreated and 6-day metronomic cyclophosphamide-treated rat 9L gliosarcoma xenografts by mouse microarray analysis to identify responsive mouse (host) cell-specific factors. Rat glioma 9L tumors were implanted sc in scid immunodeficient mice then treated with cyclophosphamide at 140 mg/kg every 6 days. Tumors were collected 6 days after the fourth cyclophosphamide treatment. Tumor RNA was then analyzed on two color Agilent mouse expression microarrays comparing cyclophosphamide-treated RNA to untreated control tumor RNA.
2015-05-04 | E-GEOD-60864 | biostudies-arrayexpress
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:Cyclophosphamide (CPA) treatment on a six-day repeating metronomic schedule induces a dramatic, innate immune cell-dependent regression of implanted gliomas. However, little is known about the underlying mechanisms of innate immune cell mobilization and recruitment, or about the role of DNA damage and cell stress response pathways in eliciting the anti-tumor immune responses linked to tumor regression. To address these questions, we compared untreated and 6-day metronomic cyclophosphamide-treated human U251 glioblastoma xenografts by human microarray analysis to identify responsive tumor cell-specific factors. Human glioma U251 tumors were implanted sc in scid immunodeficient mice then treated with cyclophosphamide at 140 mg/kg every 6 days. Tumors were collected 6 days after the second cyclophosphamide treatment and also 6 days after the third cyclophosphamide treatment. Tumor RNA was then analyzed on two color Agilent human expression microarrays comparing cyclophosphamide-treated RNA to untreated control tumor RNA.
2015-05-04 | E-GEOD-60867 | biostudies-arrayexpress
Project description:Cyclophosphamide (CPA) treatment on a six-day repeating metronomic schedule induces a dramatic, innate immune cell-dependent regression of implanted gliomas. However, little is known about the underlying mechanisms of innate immune cell mobilization and recruitment, or about the role of DNA damage and cell stress response pathways in eliciting the anti-tumor immune responses linked to tumor regression. To address these questions, we compared untreated and 6-day metronomic cyclophosphamide-treated human U251 glioblastoma xenografts by mouse microarray analysis to identify responsive mouse (host) cell-specific factors. Human glioma U251 tumors were implanted sc in scid immunodeficient mice then treated with cyclophosphamide at 140 mg/kg every 6 days. Tumors were collected 6 days after the second cyclophosphamide treatment and also 6 days after the third cyclophosphamide treatment. Tumor RNA was then analyzed on two color Agilent mouse expression microarrays comparing cyclophosphamide-treated RNA to untreated control tumor RNA.
2015-05-04 | E-GEOD-60866 | biostudies-arrayexpress