Ontology highlight
ABSTRACT:
PROVIDER: PRJNA559406 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9936780_1.fastq.gz | Fastqsanger.gz | |||
| SRR9936780_2.fastq.gz | Fastqsanger.gz | |||
| SRR9936790_1.fastq.gz | Fastqsanger.gz | |||
| SRR9936790_2.fastq.gz | Fastqsanger.gz | |||
| SRR9936781_1.fastq.gz | Fastqsanger.gz |
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Project description:Screening for urinary bladder cancer was performed in dogs in a breed (Scottish Terriers) with a very high inherited risk for bladder cancer. Naturally-occurring urothelial carcinoma in dogs serves as a relevant model for muscle invasive bladder cancer in humans. Urothelial carcinoma was detected in dogs with no outward evidence of the cancer. RNAseq data analyses were performed on these "early" tumors, and the sequencing files are included here. RNA-seq data from additional dogs has been deposited in the NCI Integrated Canine Data Commons (ICDC UBC02).
2025-03-23 | GSE199292 | GEO
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: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:In bladder, loss of mammalian Sonic Hedgehog (Shh) accompanies progression to invasive urothelial carcinoma, but the molecular mechanisms underlying this cancer-initiating event are poorly defined. Here, we show that loss of Shh results from hypermethylation of the CpG shore of the Shh gene, and that inhibition of DNA methylation increases Shh expression to halt the initiation of murine urothelial carcinoma at the early stage of progression. In full-fledged tumors, pharmacologic augmentation of Hedgehog (Hh) pathway activity impedes tumor growth, and this cancer-restraining effect of Hh signaling is mediated by the stromal response to Shh signals, which stimulates subtype conversion of basal to luminal-like urothelial carcinoma. Our findings thus provide a basis to develop subtype-specific strategies for the management of human bladder cancer.
2019-04-09 | GSE129441 | GEO
Project description:Muscle-invasive bladder cancer is closely associated with the susceptibility to metastasis and poor prognosis. In recent years, numerous studies have revealed that certain long non-coding RNAs (lncRNAs) may be involved in malignant progression of tumors. Here, we identified a lncRNA, telomerase RNA component (TERC), that is significantly upregulated in invasive bladder urothelial carcinoma tissues. We used in vitro and in vivo models to demonstrate its oncogenic effects. Mechanistically, we screened out the PPAR signaling pathway (RXRA, FABP3) regulated by TERC through proteomics and enrichment analysis.
2025-06-24 | PXD062013 | Pride
Project description:Inverted papilloma (IP) of the urinary bladder is a relatively rare neoplasm that accounts for < 1% of bladder tumor. Although generally accepted as a benign lesion, occasional reports of IP admixed with urothelial carcinoma (UC) or IP patients with synchronous or metachronous UC have raised a concern in the biologic potential of IP.
2022-05-20 | PXD027602 | Pride
Project description:Grainyhead-like transcription factor 3 (GRHL3) is known to affect cancer development depending on subtypes in various entities. Here, we analyzed the subtype-specific role of GRHL3 in bladder carcinogenesis comparing common urothelial carcinoma (UC) with squamous bladder cancers (sq-BLCA). We examined GRHL3 mRNA and protein expression in cohorts of patient samples, its prognostic role as well as its functional impact on tumorigeneses in different molecular and histopathological subtypes of bladder cancer. We showed for GRHL3 a reverse expression in squamous and urothelial bladder cancer subtypes. Stably GRHL3 overexpressing EJ28 and SCaBER in vitro models revealed a tumor suppressive function in squamous and a oncogenic role in the urothelial cancer cells affecting cell migratory and invasive capacities. Transcriptomic profiling demonstrated highly subtype specific GRHL3 regulated expression networks coined by enrichment of genes involved in integrin mediated pathways. In SCaBER loss of RhoA GTPase activity was demonstrated associated with co-regulation of EIF4E3, a potential tumor suppressor gene. Thus, our data provide for the first time a detailed insight into the role of the transcription factor GRHL3 in different histopathological subtypes of bladder cancer.
2024-06-20 | GSE241298 | GEO
Project description:Despite the increasing number of treatment options for patients with muscle-Invasive Bladder Cancer (MIBC), many of these patients ultimately have a poor prognosis. Drug responses vary considerably among patients and in many who respond initially, drug resistance may ultimately develop leading to tumor progression. Scope for improvement has been limited by the phenotypic and molecular diversity of MIBC, which impact the selection pressures of therapy. To address this translational gap, we describe the largest known canine urothelial carcinoma organoid bioarchive, with in-depth phenotypical and molecular characterization. Immunohistochemistry confirmed the expression of key biomarkers including UPKIII, E-cadherin, Vimentin, and Ki-67 in organoids. Single-nucleus RNA sequencing revealed cellular heterogeneity, while bulk RNA sequencing showed canine patient-to-patient variability in transcriptomic profiling. Bulk RNA sequencing also displayed highly similar expression profiles between tissue- and urine-derived organoids, as well as similarity to human MIBC transcriptome data. Whole genome sequencing in a subset of patients further supported the overall genomic fidelity of organoids with their tissue of origin. Finally, for proof-of concept of functional usefulness, organoid cytotoxicity to vinblastine was tested in several organoid lines. These canine bladder cancer organoid lines can be thawed, expanded, and screened for response to potential novel therapeutics to expand personalized medicine approaches. In addition, the organoid lines can serve as a valuable resource for comparative bladder cancer research, and as a pre-clinical screening tool to identify efficacious drugs before taking them into canine clinical trials to support future human clinical trials.
2025-08-30 | GSE306811 | GEO
Project description:Despite the increasing number of treatment options for patients with muscle-Invasive Bladder Cancer (MIBC), many of these patients ultimately have a poor prognosis. Drug responses vary considerably among patients and in many who respond initially, drug resistance may ultimately develop leading to tumor progression. Scope for improvement has been limited by the phenotypic and molecular diversity of MIBC, which impact the selection pressures of therapy. To address this translational gap, we describe the largest known canine urothelial carcinoma organoid bioarchive, with in-depth phenotypical and molecular characterization. Immunohistochemistry confirmed the expression of key biomarkers including UPKIII, E-cadherin, Vimentin, and Ki-67 in organoids. Single-nucleus RNA sequencing revealed cellular heterogeneity, while bulk RNA sequencing showed canine patient-to-patient variability in transcriptomic profiling. Bulk RNA sequencing also displayed highly similar expression profiles between tissue- and urine-derived organoids, as well as similarity to human MIBC transcriptome data. Whole genome sequencing in a subset of patients further supported the overall genomic fidelity of organoids with their tissue of origin. Finally, for proof-of concept of functional usefulness, organoid cytotoxicity to vinblastine was tested in several organoid lines. These canine bladder cancer organoid lines can be thawed, expanded, and screened for response to potential novel therapeutics to expand personalized medicine approaches. In addition, the organoid lines can serve as a valuable resource for comparative bladder cancer research, and as a pre-clinical screening tool to identify efficacious drugs before taking them into canine clinical trials to support future human clinical trials.
2025-08-30 | GSE306810 | GEO
Project description:We profiled two repressive histone modifications (H3K9m3 and H3K27m3) using ChIP-Seq in normal urothelial cells and cell lines representing non-invasive and invasive tumors. Two bladder cancer cell lines (RT112 and EJ/T24 from ATCC) and normal human urothelial (NHU) cells were treated according to standard ChIP-Seq protocols using antibodies against the histone modifications H3K9m3 and H3K27m3 (from Millipore). The sequencing reads were mapped against the human genome (GRCh37/hg19).
2011-08-03 | E-GEOD-31125 | biostudies-arrayexpress