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Dataset results
1,389 results for “Bladder cancer”
Epigenomic mapping identifies a super-enhancer repertoire that regulates cell identity in bladder cancers through distinct transcription factor networks [siFOXA1]
GEO Series GSE196579. Homo sapiens. 16 samples. Type: Expression profiling by high throughput sequencing.
Identification of miR-145 or miR-133a target genes in bladder cancer
GEO Series GSE19717. Homo sapiens. 4 samples. Type: Expression profiling by array.
A positive feedforward circuit shaped by DLGAP5 and E2F1 triggers bladder cancer progression
GEO Series GSE241523. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Loss of UTX/KDM6A and the activation of FGFR3 converge to regulate differentiation gene expression programs in bladder cancer [RNA-seq]
GEO Series GSE157089. Homo sapiens. 30 samples. Type: Expression profiling by high throughput sequencing.
Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells [scRNA-Seq]
GEO Series GSE176249. Homo sapiens. 1 samples. Type: Expression profiling by high throughput sequencing.
Nitazoxanide impairs mitophagy flux through ROS-mediated mitophagy initiation and lysosomal dysfunction in bladder cancer
GEO Series GSE171129. Homo sapiens. 2 samples. Type: Expression profiling by high throughput sequencing.
Recurrent inactivation of STAG2 in bladder cancer is not associated with aneuploidy [GPL6984]
GEO Series GSE51589. Homo sapiens. 6 samples. Type: SNP genotyping by SNP array; Genome variation profiling by SNP array.
Cell-free lncRNA expression signatures in urine serve as novel noninvasive biomarkers for diagnosis and recurrence prediction of bladder cancer
GEO Series GSE106074. Homo sapiens. 2 samples. Type: Expression profiling by array; Non-coding RNA profiling by array.
Epigenome analysis of parental (native) and 3-bromopyruvate-resistant UM-UC-3 bladder cancer cells
GEO Series GSE173764. Homo sapiens. 12 samples. Type: Methylation profiling by genome tiling array.
Noncoding RNA expression profiles in five pairs of bladder cancer tumor tissues and matched adjacent non-tumor tissues
GEO Series GSE190079. Homo sapiens. 10 samples. Type: Non-coding RNA profiling by high throughput sequencing.
PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity [ChIP-Seq]
GEO Series GSE201515. Homo sapiens. 6 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Hypermethylation of CpG Islands and Shores adjacent to mirtron and microRNA genes in bladder cancer
GEO Series GSE22380. Homo sapiens. 22 samples. Type: Non-coding RNA profiling by array.
Snai2-mediated upregulation of NADSYN1 promotes bladder cancer progression by interacting with PHB
GEO Series GSE243441. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
Next Generation Sequencing Quantitative Analysis of altered expression of genes in lncRNA ELNAT1 knockdown bladder cancer cells
GEO Series GSE156461. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Gene expression profile of bladder cancer cell lines treated with Mitomycin C
GEO Series GSE151505. Homo sapiens. 24 samples. Type: Expression profiling by high throughput sequencing.
Bladder-cancer-associated mutations in RXRA activate peroxisome proliferator-activated receptors to drive urothelial proliferation
GEO Series GSE107735. Homo sapiens. 18 samples. Type: Expression profiling by high throughput sequencing.
Naturally-occurring canine invasive urothelial carcinoma harbors luminal and basal transcriptional subtypes found in human muscle invasive bladder cancer
GEO Series GSE110661. Canis lupus familiaris. 33 samples. Type: Expression profiling by high throughput sequencing.
Data from: Pathology in repeated transurethral resection of a bladder tumor as a risk factor for prognosis of high-risk non-muscle-invasive bladder cancer
The prognostic value of repeat transurethral resection of bladder tumor (TURBT) in patients with diagnosed high-risk, non-muscle-invasive bladder cancer (NMIBC) was investigated. We retrospectively reviewed the medical records of patients treated from October 2004 to December 2013 at Seoul National University who underwent repeated TURBT within 2–6 weeks after an initial resection. The study enrolled patients who had been diagnosed with NMIBC at both the initial and repeat TURBT; patients with muscle-invasive tumors on repeat TURBT were excluded. We used stepwise multivariate Cox regression models stratified by study to assess the independent effects of the predictive factors and estimated hazard ratios (HRs) from the Cox models. We investigated a total of 198 patients who were diagnosed with high-risk NMIBC. In logistic regression analyses, number of bladder tumors (2–7: OR, 2.319; 8≤: OR, 3.353; p<0.05), initially high tumor grade (OR, 2.435; p = 0.040), and presence of carcinoma in situ lesion (OR, 3.639; p = 0.017) correlated with residual tumor in the repeated-TURBT specimen. T1 stage in repeated-TURBT significantly correlated with recurrence (HR, 1.837; p = 0.010) and progression (HR, 2.806; p = 0.029) in multivariate analysis. The high grades of tumors in repeated-TURBT also significantly correlated with progression but not recurrence in the multivariate analysis (HR 2.152; p = 0.008). In this study, the pathologic findings in repeated-TURBT correlated with recurrence and progression in high-risk NMIBC. Repeated-TURBT is valuable because it can predict the recurrence and progression of high-risk NMIBC in addition to obtaining accurate pathologic findings.
Exploring the Molecular Pathways of the Activation Process on PPARγ Recurrent Bladder Cancer Mutants
<p><span>The intricate involvement of Peroxisome Proliferator-Activated Receptor Gamma </span><span>(PPAR</span><span>γ</span><span>) in vital processes such as glucose homeostasis and adipogenesis is well </span><span>established. However, its multifaceted role in cancer, particularly in luminal bladder </span><span>cancer, remains a subject of intense debate. In this context, PPAR</span><span>γ</span><span>’s overexpression </span><span>and activation have been implicated in tumorigenesis. Notably, specific gain-of-function </span><span>mutations (M280I, I290M, and T475M) within PPAR</span><span>γ</span><span>’s ligand-binding domain have </span><span>been pinpointed in bladder cancer, correlating with receptor activation.</span><span> </span><span>Nonethe</span><span>less, the underlying molecular pathways prompted by these mutations remain obscure. <span>Here, we employed a dual-basin structure-based model (db SBM) to unveil the intricate </span><span>conformational dynamics that underlie the transition between PPAR</span><span>γ</span><span>’s inactive and </span><span>active states. Additionally, we explored the effects of the M280I, I290M, and T475M </span><span>mutations on this pivotal process. Our findings concur with existing literature, reveal</span><span>ing heightened ligand-independent transcriptional activity in the I290M and T475M </span><span>mutants compared to other variants.</span><span> </span><span>Importantly, both mutants displayed enhanced </span><span>stabilization of the active state relative to the wild-type receptor, and the I290M mu</span><span>tation promoted a remarkably specific transition route, rendering it a prime candidate </span><span>for further investigation. Electrostatic analysis pinpointed the pivotal role of residues </span><span>K303 and E488 in the activation cascade of I290M. This insight was substantiated by </span><span>biophysical assays, as disruption of the K303-E488 interaction curtailed the thermal </span><span>stabilization characteristic of the I290M mutation. These findings designate K303 and </span><span>E488 as potential targets for inhibitors aimed at modulating PPAR</span><span>γ</span><span> </span><span>activation, with </span><span>promising implications for refining bladder cancer prognosis. In sum, our study high</span><span>lights the remarkable predictive capabilities achieved through the integration of sim</span><span>ulation and cheminformatics methods, validated by biochemical experiments, to gain </span><span>deeper insights into molecular mechanisms of activation and identify target residues </span><span>for protein modulation.</span><br></span></p>
Early Versus Late FDG-PET/CT in Bladder Cancer
ClinicalTrials.gov study NCT03065725. IPD Sharing: NO. Countries: 1. Publications: 0.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
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DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.