Mammalia
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB17698 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Activation of oncogenic ras pathway accounts for up to 90% low-grade superficial urothelial carcinomas of bladder, and p53 deficiency is very common in high-grade muscle invasive carcinomas. These two pathways in bladder urothelial tumorigenesis used to be considered divergent and their potential collaboration has not been illustrated. We did laser capture micro-dissection (LCM) to separate the tumor cells from the whole bladder tissues from H-ras transgenic and p53 knockout mice, as well as normal urothelial cells as control. Microarray was then performed to identify distinct classes of up-regulated genes during tumorigenesis and progression. In order to get the gene expression profiles of carcinoma in situ (CIS), muscle invasive tumors and normal cells, we used LCM to purify the cells from mixture of different types of cells, and then extracted RNA for microarray. There are three groups applied in microarray, which are normal cells as control, CIS (tumor genesis) and invasive tumors (tumor progression).
2015-01-08 | E-GEOD-64756 | biostudies-arrayexpress
Project description:Purpose: The goals of this study are to compare 1. The transcription profile in KDM6A wildtype and KDM6A mutated urothelial bladder carcinoma. 2. The transcriptional changes in KDM6A mutated urothelial bladder carcinoma upon EZH2 inhibitor treatment.
2017-03-01 | GSE92723 | GEO
Project description:Activating mutations of FGFR3 are found in a high proportion of bladder tumours. The molecular consequences of FGFR3 mutation in urothelial cells and the mechanisms by which mutant FGFR3 may drive bladder tumourigenesis are largely unknown. We used expression arrays to identify downstream targets of mutant FGFR3 signalling in normal urothelial cells. TERT-immortalized normal urothelial cells stably transduced to express the most common FGFR3 mutation (S249C) were compared with control cells transduced with the empty vector (pFB).
2014-09-12 | E-GEOD-61352 | biostudies-arrayexpress
Project description:Activation of oncogenic ras pathway accounts for up to 90% low-grade superficial urothelial carcinomas of bladder, and p53 deficiency is very common in high-grade muscle invasive carcinomas. These two pathways in bladder urothelial tumorigenesis used to be considered divergent and their potential collaboration has not been illustrated. We did laser capture micro-dissection (LCM) to separate the tumor cells from the whole bladder tissues from H-ras transgenic and p53 knockout mice, as well as normal urothelial cells as control. Microarray was then performed to identify distinct classes of up-regulated genes during tumorigenesis and progression.
2015-01-08 | GSE64756 | GEO
Project description:We are using circRNA expression profiling to identify novel circular RNA regulating EMT progression in urothelial carcinoma of the bladder.
2021-04-04 | GSE112719 | GEO
Project description:Here we report the discovery of truncating mutations of the gene encoding the cohesin subunit STAG2, which regulates sister chromatid cohesion and segregation, in 36% of papillary non-invasive urothelial carcinomas and 16% of invasive urothelial carcinomas of the bladder. Our studies suggest that STAG2 has a role in controlling chromosome number but not the proliferation of bladder cancer cells. These findings identify STAG2 as one of the most commonly mutated genes in bladder cancer. Affymetrix CytoScan HD Arrays were performed according to the manufacturer's directions on genomic DNA extracted directly from 12 snap-frozen human urothelial carcinoma primary tumors with somatic mutations of the STAG2 gene.
2013-06-30 | GSE41581 | GEO
Project description:This is a comprehensive genomic characterization of 40 urothelial bladder carcinoma (UBC) cell lines including information on origin, mutation status of genes implicated in bladder cancer (FGFR3, PIK3CA, TP53, and RAS), copy number alterations assessed using high density SNP arrays, uniparental disomy (UPD) events, and gene expression. Based on gene mutation patterns and genomic changes we identify lines representative of the FGFR3-driven tumor pathway and of the TP53/RB tumor suppressor-driven pathway. High-density array copy number analysis identified significant focal gains (1q32, 5p13.1-12, 7q11, and 7q33) and losses (i.e. 6p22.1) in regions altered in tumors but not previously described as affected in bladder cell lines. We also identify new evidence for frequent regions of UPD, often coinciding with regions reported to be lost in tumors. Previously undescribed chromosome X losses found in UBC lines also point to potential tumor suppressor genes. Cell lines representative of the FGFR3-driven pathway showed a lower number of UPD events. Overall, there is a predominance of more aggressive tumor subtypes among the cell lines. We provide a cell line classification that establishes their relatedness to the major molecularly-defined bladder tumor subtypes. The compiled information should serve as a useful reference to the bladder cancer research community and should help to select cell lines appropriate for the functional analysis of bladder cancer genes, for example those being identified through massive parallel sequencing. Copy Number Variations were assessed in 45 bladder cell lines, included in the UBC-40 Urothelial Bladder Cell Line Index, with Human1M-Duov3 DNA Analysis BeadChip platform
2015-06-19 | E-GEOD-64572 | biostudies-arrayexpress
Project description:This is a comprehensive genomic characterization of 40 urothelial bladder carcinoma (UBC) cell lines including information on origin, mutation status of genes implicated in bladder cancer (FGFR3, PIK3CA, TP53, and RAS), copy number alterations assessed using high density SNP arrays, uniparental disomy (UPD) events, and gene expression. Based on gene mutation patterns and genomic changes we identify lines representative of the FGFR3-driven tumor pathway and of the TP53/RB tumor suppressor-driven pathway. High-density array copy number analysis identified significant focal gains (1q32, 5p13.1-12, 7q11, and 7q33) and losses (i.e. 6p22.1) in regions altered in tumors but not previously described as affected in bladder cell lines. We also identify new evidence for frequent regions of UPD, often coinciding with regions reported to be lost in tumors. Previously undescribed chromosome X losses found in UBC lines also point to potential tumor suppressor genes. Cell lines representative of the FGFR3-driven pathway showed a lower number of UPD events. Overall, there is a predominance of more aggressive tumor subtypes among the cell lines. We provide a cell line classification that establishes their relatedness to the major molecularly-defined bladder tumor subtypes. The compiled information should serve as a useful reference to the bladder cancer research community and should help to select cell lines appropriate for the functional analysis of bladder cancer genes, for example those being identified through massive parallel sequencing. Expression levels were assessed in 20 bladder cell lines, included in the UBC-40 Urothelial Bladder Cell Line Index, with Affymetrix U133 array platform
2015-06-19 | E-GEOD-64279 | biostudies-arrayexpress
Project description:Activating mutations of FGFR3 are found in a high proportion of bladder tumours. The molecular consequences of FGFR3 mutation in urothelial cells and the mechanisms by which mutant FGFR3 may drive bladder tumourigenesis are largely unknown. We used expression arrays to identify downstream targets of mutant FGFR3 signalling in normal urothelial cells.
2014-09-12 | GSE61352 | GEO
Project description:Urine cytologic examination is a widely used primary pathologic screening test in the diagnosis of bladder urothelial carcinoma (BLCA), however the low diagnostic accuracy remains challenging. We conducted high-throughput proteome on ten pairs of BLCA and benign urothelial lesion (BUL) to identify a supportive proteomic marker as an ancillary test in liquid based cytology (LBC).
2018-07-04 | PXD006805 | Pride