Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA356893 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Glioblastoma cell malignancy and drug sensitivity are affected by the cell of origin
| PRJNA356891 | ENA
Project description:Human expression data from Glioblastoma cell malignancy and drug sensitivity are affected by the cell of origin.
| PRJNA356892 | ENA
Project description:The cell of origin in glioblastoma is not formally proven but generally accepted to be a neural stem cell or glial precursor cell. In addition, there is also limited knowledge about the functional consequences of the cell of origin for glioblastoma development and response to therapy. We have investigated the role of cell of origin in glioblastoma by inducing glioblastomas of defined cell of origin using PDGFB in the brains of adult mice. Gene expression was analysed from cultured mouse glioblastoma cells and a mouse cell origin gene signature was extracted that we used in a cluster analysis on gene expression data from patient-derived glioblastoma cell lines.
2017-01-23 | GSE91392 | GEO
Project description:The cell of origin in glioblastoma is not formally proven but generally accepted to be a neural stem cell or glial precursor cell. In addition, there is also limited knowledge about the functional consequences of the cell of origin for glioblastoma development and response to therapy. We have investigated the role of cell of origin in glioblastoma by inducing glioblastomas of defined cell of origin using PDGFB in the brains of adult mice. Gene expression was analysed from cultured mouse glioblastoma cells and a mouse cell origin gene signature was extracted that we used in a cluster analysis on gene expression data from patient-derived glioblastoma cell lines.
2017-01-23 | GSE91391 | GEO
Project description:Glioblastoma is a universally fatal disease characterized by remarkable molecular heterogeneity. Prognostic biomarkers in glioblastoma have implications for patient management and drug development but are currently limited. In this study, we analyzed exome-wide human glioblastoma somatic copy number alteration data and discovered cytoband 6q27 as an independent poor prognostic marker across multiple glioblastoma datasets. We then combined CRISPR-Cas9 data, human spatial transcriptomic data, and human and mouse RNA sequencing data to nominate PDE10A as a potential haploinsufficient tumor suppressor in the 6q27 region. Mouse glioblastoma modeling using the RCAS/tv-a system confirmed that Pde10a suppression induced an aggressive glioma phenotype in vivo. Cell culture analysis showed that decreased Pde10a expression led to increased Pi3k/Akt signaling, a response blocked by selective Pi3k inhibitors. Single nucleus RNA sequencing from our mouse gliomas in vivo, in combination with cell culture validation showed that Pde10a suppression was associated with a proneural to a mesenchymal transition that exhibited increased cell adhesion and decreased cell migration. PDE10A loss was associated with unmethylated MGMT promoter status in human glioblastoma and resistance to temozolomide and radiation therapy in vitro. Our results indicate that patients with glioblastoma harboring PDE10A loss have worse outcomes, increased resistance to standard-of-care therapy, and potentially increased sensitivity to PI3K inhibition.
2024-09-19 | GSE243575 | GEO
Project description:Characterization of ~ 68 cell lines derived from human sarcoma and 5 normal counterpart cells, including drug sensitivity testing, gene expression profiling and microRNA expression profiling have been completed. Data and tools for searching these data will be made publicly available through the NCI Developmental Therapeutics Program. The raw data (RCC files) are provided through the GEO website. Sarcoma represents a variety of cancers at arise from cells of mesenchymal origin and have seen limited treatment advances in the last decade. Drug sensitivity data coupled with the transcription and microRNA profiles of a cohort of sarcoma cell lines may help define novel treatment paradigms.
2016-05-01 | GSE73161 | GEO
Project description:Characterization of 68 cell lines derived from human sarcoma and 5 normal counterpart cells, including drug sensitivity testing, gene expression profiling and microRNA expression profiling have been completed. Data and tools for searching these data will be made publicly available through the NCI Developmental Therapeutics Program. The raw data (.cel files ) are provided through the GEO website. Sarcoma represents a variety of cancers at arise from cells of mesenchymal origin and have seen limited treatment advances in the last decade. Drug sensitivity data coupled with the transcription and microRNA profiles of a cohort of sarcoma cell lines may help define novel treatment paradigms.
2015-08-01 | GSE68591 | GEO
Project description:Characterization of ~68 cell lines derived from human sarcoma and 5 normal counterpart cells, including drug sensitivity testing, gene expression profiling and microRNA expression profiling have been completed. Data and tools for searching these data will be made publicly available through the NCI Developmental Therapeutics Program. The raw data (RCC files) are provided through the GEO website. Sarcoma represents a variety of cancers at arise from cells of mesenchymal origin and have seen limited treatment advances in the last decade. Drug sensitivity data coupled with the transcription and microRNA profiles of a cohort of sarcoma cell lines may help define novel treatment paradigms.
2015-08-01 | GSE69470 | GEO
Project description:Genome-wide analysis of gene expression in response to bortezomib treatment(33 nM) in cell lines before and after selection for resistance. Multiple myeloma (MM) is a hematologic malignancy characterized by the proliferation of neoplastic plasma cells in the bone marrow. While the first-to-market proteasome inhibitor bortezomib/VELCADE has been successfully used to treat myeloma patients, drug resistance remains an emerging problem. In this study, we identify signatures of bortezomib sensitivity and resistance by gene expression profiling (GEP) using pairs of bortezomib-sensitive and -resistant cell lines created from the Bcl-XL/Myc double transgenic mouse model of MM. Finally, these data reveal complex heterogeneity within MM and suggest resistance to one drug class reprograms resistant clones to make them more sensitive to a distinct class of drugs. This study represents an important next step in translating pharmacogenomic profiling and may be useful for understanding personalized pharmacotherapy of MM patients. Transcript profiling timecourses after treatment with Bortezomib treatment (33nm) in Multiple Myeloma derived cell lines.
2013-07-02 | E-GEOD-41928 | biostudies-arrayexpress
Project description:Genome-wide analysis of gene expression in response to bortezomib treatment (33 nM) in cell lines before and after selection for resistance. Multiple myeloma (MM) is a hematologic malignancy characterized by the proliferation of neoplastic plasma cells in the bone marrow. While the first-to-market proteasome inhibitor bortezomib/VELCADE has been successfully used to treat myeloma patients, drug resistance remains an emerging problem. In this study, we identify signatures of bortezomib sensitivity and resistance by gene expression profiling (GEP) using pairs of bortezomib-sensitive and -resistant cell lines created from the Bcl-XL/Myc double transgenic mouse model of MM. Finally, these data reveal complex heterogeneity within MM and suggest resistance to one drug class reprograms resistant clones to make them more sensitive to a distinct class of drugs. This study represents an important next step in translating pharmacogenomic profiling and may be useful for understanding personalized pharmacotherapy of MM patients. Transcript profiling timecourses after treatment with Bortezomib treatment (33nm) in Multiple Myeloma derived cell lines.
2013-07-02 | E-GEOD-41927 | biostudies-arrayexpress