Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA257898 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:DNA methylation analysis of 68 glioblastoma specimen of patients treated within clinical trials, 5 samples of normal brain tissue (non-tumor brain) and 4 tumor-derived glioma sphere lines. The data was used to identify changes in DNA methylation which contribute to the aberrant of expression of HOX transcription factors. Our group had previously demonstrated that expression of HOX genes was associated with increased resistance to chemo-radiotherapy and worse outcome in GBM patients Keywords: Disease state comparison
2015-01-06 | GSE60274 | GEO
Project description:DNA methylation analysis of 68 glioblastoma specimen of patients treated within clinical trials, 5 samples of normal brain tissue (non-tumor brain) and 4 tumor-derived glioma sphere lines. The data was used to identify changes in DNA methylation which contribute to the aberrant of expression of HOX transcription factors. Our group had previously demonstrated that expression of HOX genes was associated with increased resistance to chemo-radiotherapy and worse outcome in GBM patients Keywords: Disease state comparison Bisulphite converted genomic DNA from the 77 samples were hybridised to the Illumina Infinium 450 Human Methylation Beadchip
2015-01-06 | E-GEOD-60274 | biostudies-arrayexpress
Project description:Glioblastoma (GBM) is the most aggressive cancer in brain and contains a high mortality ratedue to lack of effective treatment strategy. Molecular mechanisms of GBM characteristic invasive growth are urgently need to improve the poor prognosis. Via single nuclear-sequences of primary and recurrent GBM samples, level of the M3 muscarinic acetylcholine receptor (CHRM3) was significantly higher in recurrent samples. Moreover, immunohistochemical staining of an array of glioma samples showed that high levels of CHRM3 is correlated to poor prognosis of glioma, consistent with The Cancer Genome Atlas (TCGA) database. Knockdown of CHRM3 retarded glioma cell growth and invasion. In vivo assay of orthotopic glioma animal model indicated that inhibition of CHRM3 significantly suppressed glioma progression with prolonged survival time. Transcriptome analysis revealed that CHRM3 knockdown significantly reduced array of classic factors involved in cancer invasive growth including MMP1/MMP3/MMP10/MMP12 and CXCL1/CXCL5/CXCL8. Taken together, our study identified that CHRM3 is a new and important factor of GBM progression via regulation of multiple oncogenic genes and these results provide a new biomarker for prognosis and therapy of GBM patients.
2022-12-10 | GSE220083 | GEO
Project description:In this study, we developed an extensive dataset for a GBM case via the generation of polyclonal and monoclonal glioma stem cell lines from initial diagnosis, as well as from multiple sections of distant tumor locations of the deceased patient’s brain following tumor recurrence. Our analyses revealed the tissue-wide expansion of a new clone in the recurrent tumor as well as chromosome 7 gain and chromosome 10 loss as repeated genomic events in primary and recurrent disease. Moreover, chromosome 7 gain and chromosome 10 loss produced similar alterations in mRNA expression profiles in primary and recurrent tumors despite possessing other highly heterogeneous and divergent genomic alterations between the tumors. We identified ETV1 and CDK6 as putative candidate genes, and NFKB (complex), IL1B, IL6, Akt and VEGF as potential signaling regulators, as potentially central downstream effectors of chr7 gain and chr10 loss. Finally, the differences caused by the transcriptomic shift following gain of chromosome 7 and loss of chromosome 10 were consistent with those generally seen in GBM samples compared to normal brain in large-scale patient-tumor data sets.
2017-10-01 | GSE101113 | GEO
Project description:In this study, we developed an extensive dataset for a GBM case via the generation of polyclonal and monoclonal glioma stem cell lines from initial diagnosis, as well as from multiple sections of distant tumor locations of the deceased patient’s brain following tumor recurrence. Our analyses revealed the tissue-wide expansion of a new clone in the recurrent tumor as well as chromosome 7 gain and chromosome 10 loss as repeated genomic events in primary and recurrent disease. Moreover, chromosome 7 gain and chromosome 10 loss produced similar alterations in mRNA expression profiles in primary and recurrent tumors despite possessing other highly heterogeneous and divergent genomic alterations between the tumors. We identified ETV1 and CDK6 as putative candidate genes, and NFKB (complex), IL1B, IL6, Akt and VEGF as potential signaling regulators, as potentially central downstream effectors of chr7 gain and chr10 loss. Finally, the differences caused by the transcriptomic shift following gain of chromosome 7 and loss of chromosome 10 were consistent with those generally seen in GBM samples compared to normal brain in large-scale patient-tumor data sets.
2017-10-01 | GSE101110 | GEO
Project description:To investigate the role of mitochondrial metabolic pathways in glioma radioresistance, we established the radioresistant (RR) glioblastoma (GBM) cells in vitro and collected 2 self-pairs of primary and recurrent GBM samples. We then performed gene expression profiling analysis using data obtained from RNA-seq of GBM cells and tissue samples.
2023-06-01 | GSE206917 | GEO
Project description:Glioblastoma (GBM) is the most common lethal primary brain cancer in adults. Despite treatment regimens including surgical resection, radiotherapy, and temozolomide (TMZ) chemotherapy, growth of residual tumor leads to therapy resistance and death. At recurrence, a quarter to a third of all gliomas have hypermutated genomes 5, with mutational burdens orders of magnitude greater than in normal tissue. Here, we quantified the mutational landscape progression in a patient’s primary and recurrent GBM, and uncovered Cas9-targetable repeat elements. We show that CRISPR-mediated targeting of highly repetitive loci enables rapid elimination of GBM cells, an approach we term “Genome Shredding”. Importantly, in the patient’s recurrent GBM, we identified unique repeat sequences with TMZ mutational signature and demonstrate that their CRISPR targeting enables cancer-specific cell ablation. “Cancer Shredding” leverages the non-coding genome and therapy-induced mutational signatures for targeted GBM cell depletion and provides an innovative paradigm to develop treatments for hypermutated glioma.
2023-10-05 | GSE244497 | GEO
Project description:Circular RNAs are single-stranded covalently closed non-coding RNAs expressed in a variety of tissues and cells. Glioblastoma (GBM) is the most aggressive and lethal tumor in the central nervous system, characterized by high recurrence and mortality rates. Here we explore circRNA expression profiles in 26 primary and 3 recurrent GBM samples and compare them to healthy brain tissue. Additionally we compare expression of circRNA in GBM patients blood in comparison to healthy donor blood.
2024-06-29 | GSE196695 | GEO
Project description:Treating recurrent GBM is a clinical challenge due to its highly resistant and aggressive nature. In order to develop new therapeutic targets for recurrent GBM a better understanding of its molecular landscape is necessary. Here we used a cellular model, developed in our lab which generates paired primary and recurrent samples from GBM cell lines and primary patient samples hence allowing us to compare the molecular differences between the two populations. Total RNA seq analysis of parent and recurrent population of two cell lines and one patient sample revealed a significant upregulation of Extracellular matrix interaction in recurrent population. Since matrix stiffness plays a pivotal role in cell-ECM interaction and downstream signaling, we developed a system that mimicked the brain like substrate stiffness by using collagen coated polyacrylamide-based substrate whose stiffness can be modified from normal brain (0.5kPa) to tumorigenic (10kPa). Using these substrates, we were able to capture the morphological and physiological differences between parent and recurrent GBM which were not evident on plastic surfaces (~1 GPa). On 0.5kPa, unlike circular parent cells, recurrent GBM cells showed two morphologies (circular and elongated). The recurrent cells growing on 0.5kPa also showed higher proliferation, invasion, migration and in-vivo tumorigenicity in orthotropic GBM mouse model, compared to parent cells. Furthermore, recurrent cells exhibited elevated velocity irrespective of substrate stiffness, which indicated that recurrent cells may possess inherent differential mechanosignalling ability which was reflected by higher expression of ECM proteins like Collagen IVA, MMP2 and MMP9. Moreover, mice brain injected with recurrent cells grown on 0.5kPa substrate showed higher Young’s modulus values suggesting that recurrent cells conditioned on 0.5kPa make the surrounding ECM stiffer. Importantly, inhibition of EGFR signaling, that is amplified with tissue stiffening in GBM resulted in decreased invasion, migration and proliferation in 0.5kPa recurrent cells, but interestingly survival remained unaffected, highlighting the importance of mimicking the physiological stiffness of the brain mimicking clinical scenario. Total RNA seq analysis of parent and recurrent cells grown on plastic and 0.5kPa substrate identified PLEKHA7 as significantly upregulated gene specifically in 0.5kPa recurrent sample. Higher protein expression of PLEKHA7 in recurrent GBM as compared to primary GBM was validated in patient biopsies. Accordingly, PLEKHA7 knockdown reduced invasion and survival of recurrent GBM cells. Together, these data provides a model system that captures the differential mechanosensing signals of primary and recurrent GBM cells and identifies a novel potential target specific for recurrent GBM.
2023-06-29 | E-MTAB-11293 | biostudies-arrayexpress
Project description:We compared whole genome expression profiles of GSCs with normal human cortex, human neural stem cells (hNSC) from fetal cortex, glioblastoma (GBM) primary, and recurrent tumors to find GSC-specific plasma membrane transcripts. All of the expression profiles were batch normalized by a robust multichip average (RMA) algorithm using Geospiza GeneSifter (PerkinElmer) online microarray database and analysis software. The data was then exported into Microsoft Office Excel 2010 and organized for GSC transcripts with raw intensity values 10 fold or higher over normal brain, hNSCs, GBM primary and recurrent tumor samples. The reverse sorting algorithm was done to obtain downregulated GSC trascripts.
2013-11-14 | E-GEOD-51822 | biostudies-arrayexpress