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Dataset results
1,389 results for “bladder cancer”
Intrinsic higher potency of basal urothelial cells to intermediate and umbrella cells as the cell of origin for bladder cancer
GEO Series GSE305544. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
High glucose associated YTHDC1 lactaylation reduces the sensitivity of bladder cancer to enfortumab vedotin therapy
GEO Series GSE291592. Homo sapiens. 4 samples. Type: Expression profiling by high throughput sequencing.
N6-methyladenosine RNA modification drives a rapid shift to cisplatin resistance in bladder cancer by regulating SLC7A11 expression via YTHDF3 [RNA-seq]
GEO Series GSE231835. Homo sapiens. 10 samples. Type: Expression profiling by high throughput sequencing.
RNA sequencing data for 30 bladder cancer cell lines
GEO Series GSE97768. Homo sapiens. 30 samples. Type: Expression profiling by high throughput sequencing.
Asparagine regulates RIG-I stability to suppress anti-tumor immunity in bladder cancer
GEO Series GSE270353. Mus musculus. 3 samples. Type: Expression profiling by high throughput sequencing.
Gene expression analysis in bladder cancer cells lines
GEO Series GSE28255. Homo sapiens. 12 samples. Type: Expression profiling by array.
High-throughput Sequencing Quantitative Analysis of altered genes expression in bladder cancer with anti-PD-1 treatment
GEO Series GSE272539. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
N-acetyltransferase 10 drives cisplatin chemoresistance by enhancing ac4C-associated DNA repair in bladder cancer
GEO Series GSE200285. Homo sapiens. 16 samples. Type: Expression profiling by high throughput sequencing; Other.
Identification and regulation of circulating tumor TCR-matched cytotoxic CD4+ lymphocytes by KLRG1 in bladder cancer
GEO Series GSE293860. Homo sapiens. 106 samples. Type: Expression profiling by high throughput sequencing; Other.
Genome-wide analysis of gene expression in bladder cancer cell lines 253JB-V and UM-UC13 exposed to bortezomib
GEO Series GSE46132. Homo sapiens. 8 samples. Type: Expression profiling by array.
Human bladder cancer cell line high throughput sequencing - genes regulated by hMSH2 - CDDP therapy
GEO Series GSE193753. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
GRIK2 is a target for bladder cancer stem-like cell-targeting immunotherapy
GEO Series GSE166947. Homo sapiens. 7 samples. Type: Expression profiling by high throughput sequencing.
Dataset related to article "Assessing the Feasibility and Accuracy of High-resolution Microultrasound Imaging for Bladder Cancer Detection and Staging"
<p>BACKGROUND:</p> <p>Magnetic resonance imaging (MRI) has been proposed as a staging tool for bladder cancer (BC), but its use has been limited by its high costs and limited availability. Microultrasound (mUS) is a novel technology capable of providing high-resolution images of the prostate.</p> <p>OBJECTIVE:</p> <p>To test the feasibility of high-resolution mUS in patients diagnosed with BC and its ability to differentiate between non-muscle-invasive BC (NMIBC) and muscle-invasive BC (MIBC).</p> <p>DESIGN, SETTING, AND PARTICIPANTS:</p> <p>This is an observational prospective study performed in 23 patients with a diagnosis of primary BC scheduled for an endoscopic treatment.</p> <p>SURGICAL PROCEDURE:</p> <p>Micro-US was performed before transurethral resection of bladder tumor using the ExactVu system with an EV29L 29-MHz side-fire transducer (Exact Imaging, Markham, Canada).</p> <p>MEASUREMENTS:</p> <p>The endpoints were to test the feasibility, describe the normal bladder wall anatomy, identify the lesions, and compare the mUS findings with the histopathological results.</p> <p>RESULTS AND LIMITATIONS:</p> <p>Micro-US was accurate in differentiating the three layers of the bladder wall in all cases. Bladder cancers were clearly identified as heterogeneous structures protruding from the normal bladder wall. In 14 cases the lesions appeared confined to the lamina propria, and in all cases NMIBC was confirmed by the final pathological report. In the other patients, the lesions seemed to extend into the muscular layer, but MIBC was confirmed in five out of seven cases (71.4%) from the pathologist. The small sample size was the main limitation of the current study.</p> <p>CONCLUSIONS:</p> <p>Our findings showed that mUS is able to differentiate the bladder wall layers and identify the bladder cancer stage. Further studies with a larger population and imaging correlation with MRI are warranted before its introduction in clinical practice.</p> <p>PATIENT SUMMARY:</p> <p>In this report, a new imaging technique was tested for the characterization of bladder cancer. Microultrasound appears to be feasible and capable of discriminating between superficial and invasive tumors</p>
Dataset related to article "Stereotactic Body Radiation Therapy in the Management of Oligometastatic and Oligoprogressive Bladder Cancer and Other Urothelial Malignancies"
<p>This record contains raw data related to article "Stereotactic Body Radiation Therapy in the Management of Oligometastatic and Oligoprogressive Bladder Cancer and Other Urothelial Malignancies"</p> <p><strong>Aims: </strong>Bladder cancer represents the most common type of urothelial carcinoma, with a median overall survival of 12.5-15 months in the case of metastatic disease. We evaluated the role of stereotactic body radiation therapy (SBRT) in the management oligometastatic urothelial cancer.</p> <p><strong>Materials and methods: </strong>Data on patients with a maximum of five metastases were collected from three institutions. Concomitant systemic therapy was allowed. End points were the local control of treated metastases, distant progression-free survival (PFS), overall PFS and overall survival.</p> <p><strong>Results: </strong>Data for 82 lesions and 61 patients were included. The primary tumour was located in the bladder in 82% of patients, followed by kidney pelvis (11.5%). The most common treated site was lung (40.2%). Twenty-nine (47.5%) and 14 (23%) patients received systemic therapy before and during SBRT, respectively. The median BED10 value was 78.7 Gy. The median follow-up was 17.2 months. Rates of local control at 1 and 2 years were 92% and 88.9%, respectively, with correlation with systemic therapy before SBRT (hazard ratio 2.62, P = 0.034). Overall PFS at 1 and 2 years was 47.9% and 38.1%, respectively. The number of metastases was a predictive factor (hazard ratio 2.65, P = 0.008). The median overall survival was 25.6 months. Total dose (hazard ratio 0.93, P = 0.003) and BED10 (hazard ratio 0.97, P = 0.006) were correlated with overall survival. No grade ≥2 adverse events were reported.</p> <p><strong>Conclusions: </strong>SBRT represents an effective and safe treatment in metastatic urothelial carcinoma. Prospective randomised trials are necessary to better evaluate the benefit on delaying the onset of new systemic therapies.</p>
ACSL5 Regulated Acetyl-CoA to Promote Bladder Cancer Cellular Senescence via 53BP1 Acetylation
<p><span>Disruption of the fatty acid oxidation process (FAO) significantly affects the tumorigenesis of bladder cancer (BC). Apart from energy regulation, acetyl-CoA from FAO, as an important substrate for protein acetylation, plays an important role in BC. Here, we found that long-chain fatty acid synthase 5 (ACSL5) acting as a key enzyme in the initial stage of <span> </span>FAO, was downregulated in BC, and the decreased level of ACSL5 was strongly associated with a poor prognosis for BC patients. We found that the main reason for the low expression of ACSL5 in BC is the highly methylated CpG islands in its DNA, which is closely regulated by DNA methyltransferase 1 (DNMT1). Upregulating ACSL5 expression in BC cells significantly promoted FAO, and reduces the intracellular lipid content while increasing the level of acetyl-CoA. We demonstrated that restoration of ACSL5 expression promoted K1360 acetylation of TP53-binding protein 1 (53BP1), through posttranslational modification (PTM), subsequently enhancing the recruitment of the P53-P21 senescent signaling axis in the nucleus and promoting cellular senescence. In vivo and in vitro, ACSL5 overexpression promoted BC senescence and inhibited BC cell proliferation, and elaidic acid (EA) feeding further enhanced these effects. In summary, our study revealed that ACSL5-mediated lipid oxidation reduces the intracellular lipid content, promotes cellular senescence, and inhibits the proliferation of BC. The activation of ACSL5-mediated lipid oxidation to regulate cellular senescence may provide an innovative direction for BC therapy.</span></p>
Dataset related to article "Xpert Bladder Cancer Monitor May Avoid Cystoscopies in Patients Under "Active Surveillance" for Recurrent Bladder Cancer (BIAS Project): Longitudinal Cohort Study "
<p>This record contains raw data related to article “Xpert Bladder Cancer Monitor May Avoid Cystoscopies in Patients Under "Active Surveillance" for Recurrent Bladder Cancer (BIAS Project): Longitudinal Cohort Study"</p> <p>Abstract</p> <p><strong>Objectives: </strong> To test the hypothesis that patients under active surveillance (AS) for Non-muscle Invasive Bladder Cancer (NMIBC) who were negative on longitudinal re-testing by the Xpert<sup>®</sup> Bladder Cancer Monitor (Xpert BC Monitor) assay may avoid unnecessary cystoscopies and urine cytology (UC).</p> <p><strong>Subjects/patients or materials and methods: </strong> This is a prospective cohort study of patients enrolled in the AS protocol for recurrent NMIBC (Bladder Cancer Italian Active Surveillance, BIAS project), whose urine samples were analyzed by Xpert BC Monitor upon entry in the study (T0). Patients who had a negative Xpert test and did not fail AS, underwent additional Xpert tests after 4 (T1), 8 (T2), and 12 (T3) months. The clinical utility of Xpert was assessed by determining the number of cystoscopies and UC that could be avoided within 1 year.</p> <p><strong>Results: </strong> Overall, 139 patients were tested with Xpert at T0. Median follow-up was 23 (IQR 17-27) months. Sixty-eight (48.9%) patients failed AS, 65 (46.7%) are currently on AS, and 6 (4.3%) were lost at follow-up. At T0 57 (41.0%) patients had a negative test and 36 (63.2%) are still in AS. In patients with 2 consecutives negative Xpert tests, we could have avoided 73.9% of unnecessary cystoscopies, missing 26.4% failure, up to avoid all cystoscopies with 4 negative tests missing only 12% of failure. All the patients with negative Xpert had negative UC. Failure-free-survival at median follow-up (23 month) stratified for having 0, 1, or ≥2 negative tests was 67.0, 55.1. and 84.1, respectively.</p> <p><strong>Conclusion: </strong> Our findings suggest that Xpert BC Monitor assay, when it is longitudinally repeated, could significantly reduce the number of unnecessary cystoscopies and UC during their follow-up.</p> <p> </p>
Dataset related to article "Intratumoral Switch of Molecular Phenotype and Overall Survival in Muscle Invasive Bladder Cancer"
<p>This record contains raw data related to article “Intratumoral Switch of Molecular Phenotype and Overall Survival in Muscle Invasive Bladder Cancer"</p> <p>Abstract</p> <p>In recent years, immunohistochemical protein expression was studied as a surrogate to the molecular classification of bladder cancer, although no tissue biomarkers are available for clinical use to predict survival or the response to neoadjuvant chemotherapy (CT) in UC, as the literature produced conflicting results. This retrospective study included TURB specimens harboring foci of HG pT2 muscle-invasive bladder carcinoma (MIBC) from 251 patients who subsequently underwent radical cystectomy. We performed immunohistochemical analysis on tumor samples, for relevant gene-expression-based markers for basal type (<em>CD44</em>, <em>CK5/6</em>) and luminal type (<em>CK20</em> and <em>pPARγ</em>). Piescore, investigated in both non-muscle-invasive (NMI) and muscle-invasive (MI) components of the tumor, divided basal and luminal UC-types when at least three of the four markers were consistent with a specific phenotype, mixed types if one/two luminal and basal markers were present simultaneously, and neu-like types when all four markers investigated were negative. Eighteen selected cases were also investigated with RT-PCR to validate, and to increase the specificity of, the immunohistochemical results. We observe an immunophenotypical difference in the NMI and MI components in 96/251 UC patients (38.25%): half of tumors (44/96 cases) have a transition to basal, 36.46% (35/96 cases) to neu-like, 12.5% (12/96 cases) to mixed, and 5.2% (5/96 cases) to luminal phenotypes. Mixed tumors in the NMI component are more likely to change phenotype than other groups, particularly compared with basal tumors, which demonstrate greater stability (only 8/96 cases, <em>p</em> &lt; 0.00001). The transition of luminal tumors to basal display a better OS compared with the transition toward neu-like tumors (<em>p</em> = 0.027). Overall, the phenotypical switch does not affect lymphovascular invasion, pT, DFS, or OS compared with non-switched cases. In the MI component, the presence of <em>CD44</em> expression, irrespective of score-related phenotype, shows a protective effect in papillary-type UC (OS <em>p</em> = 0.008, HR 0.453, PFS <em>p</em> = 0.07, HR 0.599), and in UC naïve for CT (<em>p</em> = 0.0479). Piescore immunophenotyping reveals an intratumoral phenotypical transition between the NMI and MI components of the same tumor. The molecular change is a common event in the mixed and luminal categories, but not in basal tumors, which show better phenotypical stability. This phenomenon could partially explain the sensitivity of a subset of luminal UC to chemotherapy: good responders could be "non-real" luminal UC, which acquire nasal markers, such as <em>CD44</em>.</p>
An Expanded Access Study of Bemarituzumab (FPA144) for a Single Patient With Recurrent Bladder Cancer
ClinicalTrials.gov study NCT03801278. IPD Sharing: Not stated. Countries: 0. Publications: 0.
Effect of EZH2 inhibition on ARID1A mutant bladder cancer cell lines
GEO Series GSE150249. Homo sapiens. 4 samples. Type: Expression profiling by array.
Genome-wide synthetic lethal Crispr screen identifies SRM as a target that enhances erdafitinib efficacy in FGFR-mutant bladder cancer
GEO Series GSE276411. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
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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)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
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.