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Urothelial-to-Neural Lineage Plasticity Drives Progression to Small Cell Bladder Cancer

ABSTRACT: Urothelial-to-Neural Lineage Plasticity Drives Progression to Small Cell Bladder Cancer

PROVIDER: PRJNA606528 | ENA |

REPOSITORIES: ENA

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Urothelial-to-Neural Lineage Plasticity Drives Progression to Small Cell Bladder Cancer [RNA]

Project description:Urothelial-to-Neural Lineage Plasticity Drives Progression to Small Cell Bladder Cancer [RNA]

| PRJNA606532 | ENA

Urothelial-to-Neural Lineage Plasticity Drives Progression to Small Cell Bladder Cancer [miRNA]

Project description:Urothelial-to-Neural Lineage Plasticity Drives Progression to Small Cell Bladder Cancer [miRNA]

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Multi Lineage Heterogeneity and Plasticity in Urothelial Carcinoma of the Bladder

Project description:Multi Lineage Heterogeneity and Plasticity in Urothelial Carcinoma of the Bladder

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Urothelial-to-Neural Plasticity Drives Progression to Small Cell Bladder Cancer.

Project description:We report a comprehensive molecular analysis of 34 cases of small cell carcinoma (SCC) and 84 cases of conventional urothelial carcinoma (UC), with The Cancer Genome Atlas cohort of 408 conventional UC bladder cancers used as the reference. SCCs showed mutational landscapes characterized by nearly uniform inactivation of TP53 and were dominated by Sanger mutation signature 3 associated with loss of BRCA1/2 function. SCCs were characterized by downregulation of luminal and basal markers and were referred to as double-negative. Transcriptome analyses indicated that SCCs displayed lineage plasticity driven by a urothelial-to-neural phenotypic switch with a dysregulated epithelial-to-mesenchymal transition network. SCCs were depleted of immune cells, and expressed high levels of the immune checkpoint receptor, adenosine receptor A2A (ADORA2A), which is a potent inhibitor of immune infiltration. Our observations have important implications for the prognostication and development of more effective therapies for this lethal bladder cancer variant.

| S-EPMC7286965 | biostudies-literature

Urothelial-to-Neural Lineage Plasticity Drives Progression to Small Cell Bladder Cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-10-01 | GSE145261 | 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

Urothelial-to-Neural Lineage Plasticity Drives Progression to Small Cell Bladder Cancer [RNA]

Project description:We report a comprehensive molecular analysis of 22 cases of SCC

2020-10-01 | GSE145260 | GEO

Urothelial-to-Neural Lineage Plasticity Drives Progression to Small Cell Bladder Cancer [miRNA]

Project description:We report a comprehensive molecular analysis of 22 cases of SCC

2020-10-01 | GSE145259 | GEO

Single cell transcriptomes of mouse bladder urothelium uncover novel cell type markers and urothelial differentiation characteristics.

Project description:Objectives: Much of the information to date in terms of subtypes and function of bladder urothelial cells were derived from anatomical location or by the expression of a small number of marker genes. To have a comprehensive map of the cellular anatomy of bladder urothelial cells, we performed single-cell RNA-sequencing to thoroughly characterize mouse bladder urothelium. Materials and methods: A total of 18,917 single cells from mouse bladder urothelium was analyzed by unbiased single-cell RNA sequencing. The expression of the novel cell marker was confirmed by immunofluorescence using urinary tract infections models. Results: Unsupervised clustering analysis identified 8 transcriptionally distinct cell subpopulations from mouse bladder urothelial cells. We discovered a novel type of bladder urothelial cells marked by Plxna4 that may be involved with host response and wound healing. We also found a group of basal-like cells labeled by ASPM that could be the progenitor cells of adult bladder urothelium. ASPM+ urothelial cells are significantly increased after injury by UPEC. In addition, specific transcription factors were found to be associated with urothelial cell differentiation. At the last, a number of interstitial cystitis/bladder pain syndrome-regulating genes were found differentially expressed among different urothelial cell subpopulations. Conclusions: Our study provides a comprehensive characterization of bladder urothelial cells, which is fundamental to understanding the biology of bladder urothelium and associated bladder disease.

2020-12-12 | GSE163029 | 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