Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE145261 | GEO | 2020/10/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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 [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

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

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

| PRJNA606528 | ENA

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]

| PRJNA606533 | ENA

Lineage Plasticity in Cancer Progression and Treatment.

Project description:Historically, it has been widely presumed that differentiated cells are determined during development and become irreversibly committed to their designated fates. In certain circumstances, however, differentiated cells can display plasticity by changing their identity, either by dedifferentiation to a progenitor-like state or by transdifferentiation to an alternative differentiated cell type. Such cellular plasticity can be triggered by physiological or oncogenic stress, or it can be experimentally induced through cellular reprogramming. Notably, physiological stresses that promote plasticity, such as severe tissue damage, inflammation, or senescence, also represent hallmarks of cancer. Furthermore, key drivers of cellular plasticity include major oncogenic and tumor suppressor pathways and can be exacerbated by drug treatment. Thus, plasticity may help cancer cells evade detection and treatment. We propose that cancer can be considered as a disease of excess plasticity, a notion that has important implications for intervention and treatment.

| S-EPMC5942183 | biostudies-literature

FOXA1 repression drives lineage plasticity and immune heterogeneity in bladder cancers with squamous differentiation.

Project description:Cancers arising from the bladder urothelium often exhibit lineage plasticity with regions of urothelial carcinoma adjacent to or admixed with regions of divergent histomorphology, most commonly squamous differentiation. To define the biologic basis for and clinical significance of this morphologic heterogeneity, here we perform integrated genomic analyses of mixed histology bladder cancers with separable regions of urothelial and squamous differentiation. We find that squamous differentiation is a marker of intratumoral genomic and immunologic heterogeneity in patients with bladder cancer and a biomarker of intrinsic immunotherapy resistance. Phylogenetic analysis confirms that in all cases the urothelial and squamous regions are derived from a common shared precursor. Despite the presence of marked genomic heterogeneity between co-existent urothelial and squamous differentiated regions, no recurrent genomic alteration exclusive to the urothelial or squamous morphologies is identified. Rather, lineage plasticity in bladder cancers with squamous differentiation is associated with loss of expression of FOXA1, GATA3, and PPARG, transcription factors critical for maintenance of urothelial cell identity. Of clinical significance, lineage plasticity and PD-L1 expression is coordinately dysregulated via FOXA1, with patients exhibiting morphologic heterogeneity pre-treatment significantly less likely to respond to immune checkpoint inhibitors.

| S-EPMC9630410 | biostudies-literature

FOXA2/AP-1 drives prostate cancer lineage plasticity

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

2024-04-22 | GSE232555 | 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