Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of subsets of urothelial carcinoma

ABSTRACT: Identification of bladder cancer subsets

ORGANISM(S): Homo sapiens

PROVIDER: GSE48075 | GEO | 2014/02/10

SECONDARY ACCESSION(S): PRJNA209058

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Identification of subsets of urothelial carcinoma

Project description:Identification of bladder cancer subsets 142 primary bladder tumors including superficial and invasive tumors were arrayed. 73 invasive tumors out of 142 tumors were used for muscle invasive baldder cancer classification

2014-02-10 | E-GEOD-48075 | biostudies-arrayexpress

Gene expression profiling of urothelial carcinoma

Project description:Identification of bladder cancer subsets 128 FFPE bladder tumors were used to validate the bladder cancer subsets

2014-02-10 | E-GEOD-48276 | biostudies-arrayexpress

Gene expression profiling of urothelial carcinoma

Project description:Identification of bladder cancer subsets

2014-02-10 | GSE48276 | GEO

Molecular subtype classification of urothelial carcinoma in Lynch syndrome

Project description:We aimed to provide a molecular description of Lynch syndrome-associated urothelial cancer in relation to molecular subtypes of sporadic bladder cancer. Whole genome mRNA expression profiles of 41 tumors and immunohistochemical stainings against FGFR3, KRT5, CCNB1, RB1, and CDKN2A (p16) of 37 tumors from Lynch syndrome patients were generated. Pathological data, microsatellite instability, anatomic location, and overall survival data was analyzed and compared with data from sporadic bladder cancer.

2019-01-01 | GSE104922 | GEO

Multi Lineage Heterogeneity and Plasticity in Urothelial Carcinoma of the Bladder

Project description:Single cell transcriptome analyses of mouse and human model systems of bladder cancer

2020-03-01 | GSE146137 | GEO

Transcriptome analysis for KDM6A mutated urothelial bladder carcinoma and EZH2 inhibitor treated KDM6A mutated urothelial bladder carcinoma

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

Cisplatin resistance driver gene CLSPN product is a target for immunotherapy in urothelial carcinoma.

Project description:Bladder cancer is a major and mortal disease in urological area. Cisplatin is a key drug for bladder cancer especially for muscle invasive cases. In most cases of bladder cancer, cisplatin is effective; however, resistance to cisplatin is critical for patient’s prognosis. Thus, treatment strategy for cisplatin resistant bladder cancer is essential to improve current prognosis. In this study, we established cisplatin resistant bladder cancer line (CR cells) using a urothelial carcinoma line UM-UC-3 cells. We screened potential targets for CR cells and found that claspin is overexpressed in CR cells. Claspin mRNA knockdown revealed that claspin has a role in cisplatin resistance in CR cells. In our previous study, we found HLA-A*02:01-restricted CLSPN peptide by an HLA ligandome analysis. We thus generated CLSPN peptide specific CTL clone and found that CLSPN peptide-specific CTL clone recognized CR cells at higher levels compared with that of UM-UC-3 wild type cells. These findings indicate that claspin is a driver for cisplatin resistance and claspin peptide-specific immunotherapy is effective for cisplatin resistant cases.

2024-04-10 | GSE217413 | GEO

To elucidate the role of Protein Kinase C in Urothelial Bladder Carcinoma.

Project description:Comprehensive evaluation of human cell lines for the transcription dynamics in response to the inhibition of PKC isozymes ε & ζ in bladder cancer.

2024-10-30 | GSE245118 | GEO

Loss of YTHDC1 m6A reading function promotes invasiveness in urothelial carcinoma of the bladder [RNA-seq]

Project description:Bladder cancer poses significant clinical challenges due to its high metastatic potential and poor prognosis, especially when it progresses to muscle-invasive stages. Here, we show that the m6A reader YTHDC1 is downregulated in muscle-invasive bladder cancer and is negatively correlated with the expression of epithelial‒mesenchymal transition genes. The functional inhibition or depletion of YTHDC1 increased the migration and invasion of urothelial cells. Integrative analysis of multimodal sequencing datasets provided detailed insights into the molecular mechanisms mediating YTHDC1-dependent phenotypes and identified SMAD6 as a key transcript involved in the invasiveness of urothelial carcinoma of the bladder. Notably, SMAD6 mRNA colocalized less with YTHDC1 in tumoral tissues than in paratumoral tissues, indicating disrupted binding during cancer progression. Our findings establish YTHDC1-dependent m6A reading as a critical epitranscriptomic mechanism regulating bladder cancer invasiveness and provide a paradigm for the epitranscriptomic deregulation of cancer-associated networks.

2024-12-16 | GSE266223 | GEO