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1,389 results for “Bladder cancer”
Gemcitabine Hydrochloride and Cisplatin Before Surgery in Treating Patients With Muscle Invasive Bladder Cancer
ClinicalTrials.gov study NCT01611662. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Deep Learning Radiomics Model for Predicting Post-cystectomy Outcome in Muscle Invasive Bladder Cancer
ClinicalTrials.gov study NCT06092450. IPD Sharing: NO. Countries: 1. Publications: 1.
Relationship Between Tumor Mutation Burden and Predicted Neo-antigen Burden in Patients With Advanced Melanoma or Bladder Cancer Treated With Nivolumab or Nivolumab Plus Ipilimumab (CA209-260)
ClinicalTrials.gov study NCT02553642. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Pembrolizumab With Chemoradiotherapy as Treatment for Muscle Invasive Bladder Cancer
ClinicalTrials.gov study NCT02662062. IPD Sharing: NO. Countries: 1. Publications: 1.
4B951, Combination Chemotherapy in Treating Patients With Bladder Cancer
ClinicalTrials.gov study NCT00005047. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Neuromuscular Blockade During Transurethral Resection of Bladder Cancer
ClinicalTrials.gov study NCT03039543. IPD Sharing: UNDECIDED. Countries: 1. Publications: 3.
Study of Ferumoxytol Enhanced MRI for Detecting Lymph Node Metastases in Prostate, Bladder, and Kidney Cancers
ClinicalTrials.gov study NCT02141490. IPD Sharing: NO. Countries: 1. Publications: 3.
Study to Improve Detection and Early Recurrence Rate in Bladder Cancer Patients Using Hexvix Fluorescence Cystoscopy
ClinicalTrials.gov study NCT00233402. IPD Sharing: Not stated. Countries: 5. Publications: 1.
CAVATAK (CVA21) in Non-muscle Invasive Bladder Cancer (VLA-012 CANON)
ClinicalTrials.gov study NCT02316171. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Phase II Trial Evaluating an Organ-conserving Strategy by Radiochemotherapy for Muscle-infiltrative Bladder Cancer
ClinicalTrials.gov study NCT01495676. IPD Sharing: NO. Countries: 1. Publications: 26.
Mitomycin C With Hyperthermia and Intravesical Mitomycin C to Treat Recurrent Bladder Cancer
ClinicalTrials.gov study NCT00734994. IPD Sharing: Not stated. Countries: 1. Publications: 3.
A Study of Atezolizumab Compared With Chemotherapy in Participants With Locally Advanced or Metastatic Urothelial Bladder Cancer [IMvigor211]
ClinicalTrials.gov study NCT02302807. IPD Sharing: Not stated. Countries: 29. Publications: 7.
Data from: MFSD12, transcriptionally regulated by PLAGL2, promotes bladder cancer progression
Open the record for dataset details and reuse information.
Arsenic (+3 oxidation state) methyltransferase gene polymorphisms and expression on bladder cancer
<p><span><span><span><span>Inorganic arsenic (iAs) is a recognized environment-related factor for bladder cancer (BCa). </span><span><span>Arsenic (+3 oxidation state) methyltransferase (</span></span><i><span><span>AS3MT</span></span></i><span><span>)</span></span><i><span><span> gene</span></span></i><span> might influence BCa by regulating iAs metabolism. </span>The objectives of the present study were to systematically review eligible case-control studies about <i><span>AS3MT</span></i><i> </i>polymorphisms and BCa and to further compare the genotype distribution and allele distribution between BCa patients and controls by meta-analysis for humans. Besides, to clarify the effects of <i><span>AS3MT </span></i>expression on BCa clinical outcomes and survival time, we also conducted a series of analyses based on The Cancer Genome Atlas (TCGA) dataset. <span>Databases were systematically retrieved and we applied Stata software to perform meta-analysis. The registration of this study protocol is at PROSPERO and ID is CRD42019133947. Five articles</span> <span>were recruited and pooled results demonstrated that</span> <span>rs3740393 and rs11191438 polymorphisms were related to BCa risk in overall population (P<0.05)</span> <span>in the overall population.</span><span> In addition, GG and GC genotypes in rs3740393 and GG genotype in rs11191438 might be the susceptibility genotypes for BCa. </span><span>Results based on </span><span>168</span><span> BCa samples from TGCA indicated that patients with higher expression of </span><i><span><span>AS3MT</span></span></i><span> had poor </span><span>overall survival</span><span> time</span><span> and </span><i><span><span>AS3MT</span></span></i><span> expression is an independent indicator</span><span> for BCa </span><span>survival.</span> <span>This study identified that </span><i><span><span>AS3MT</span></span></i><span> polymorphisms could </span><span>affect</span><span> BCa risk and </span><i><span><span>AS3MT</span></span></i><span> expression was pivotal in prognosis of BCa.</span></span></span></span></p>
m6A-dependent 7-dehydrocholesterol reductase facilitates bladder cancer metastasis via cAMP/PKA/FAK axis
<p><span>Cholesterol homeostasis dysregulation </span><span>appears</span><span> in multiple tumors. However, the specific processes that cause abnormal cholesterol metabolism to affect the invasion and metastasis of bladder cancer (BC) are still unclear. In our investigation, we found a notable rise in the expression of 7-dehydrocholesterol reductase (DHCR7), a key enzyme involved in the synthesis of cholesterol, within BC tissues in comparison to normal tissues and correlated to the invasion and metastasis of BC. This elevated expression of DHCR7 in BC was attributed to the decreased degradation of mRNA mediated by YTHDF2. We discovered that DHCR7 </span><span>plays</span><span> a role in promoting bladder cancer invasion and metastasis </span><span>by</span><span> activating the cAMP-PKA-FAK pathway. Specifically, DHCR7 was found to increase the levels of cAMP by enhancing cholesterol content in lipid rafts, thereby facilitating the transduction of signaling pathways mediated by cAMP receptors. Additionally, DHCR7 was found to enhance the cAMP signaling pathway by reducing the concentration of 7-DHC and promoting the transcription of GIPR. Overall, our findings demonstrated that DHCR7 plays a crucial role in BC invasion and metastasis by modulating cholesterol synthesis and cAMP signaling pathways. Furthermore, AY9944, which acts as an inhibitor of DHCR7, shows promise as a viable therapeutic strategy for the suppression of invasion and metastasis in BC.</span></p>
The impact of genetic variants in the CYP2C8 gene on bladder cancer susceptibility 1 Short Title:Genetic variants on bladder cancer
<p>Four SNPs including rs1934953, rs1934951, rs2275620, and rs17110453 in the CYP2C8 gene were selected and determined in 550 healthy subjects and 217 bladder cancer patients. SNPs genotyping was determined using Agena MassARRAY iPLEX platform.</p>
Word folder for images in research paper titled "INSILICO MODELING OF BLADDER CANCER ASSOCIATED PROTEIN"
<p>Bladder cancer is one of several types of cancer arising from the tissues of the urinary bladder. It is a disease in which cells grow abnormally and have the potential to spread to other parts of the body. In the study a<span> 3D model was obtained using multiple templates. </span>The stereo chemical quality of the model was assessed using RAMACHANDRAN PLOT analysis. The attached word file contains the images and plots pertaining to this study.</p> <p> </p> <p> </p>
Exploring the Molecular Pathways of the Activation Process on PPARγ Recurrent Bladder Cancer Mutants
<p>The intricate involvement of Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) in vital processes such as glucose homeostasis and adipogenesis is well established. However, its multifaceted role in cancer, particularly in luminal bladder cancer, remains a subject of intense debate. In this context, PPARγ’s overexpression and activation have been implicated in tumorigenesis. Notably, specific gain-of-function mutations (M280I, I290M, and T475M) within PPARγ’s ligand-binding domain have been pinpointed in bladder cancer, correlating with receptor activation. Nonetheless, the underlying molecular pathways prompted by these mutations remain obscure. Here, we employed a dual-basin structure-based model (db SBM) to unveil the intricate conformational dynamics that underlie the transition between PPARγ’s inactive and active states. Additionally, we explored the effects of the M280I, I290M, and T475M mutations on this pivotal process. Our findings concur with existing literature, revealing heightened ligand-independent transcriptional activity in the I290M and T475M mutants compared to other variants. Importantly, both mutants displayed enhanced stabilization of the active state relative to the wild-type receptor, and the I290M mutation promoted a remarkably specific transition route, rendering it a prime candidate for further investigation. Electrostatic analysis pinpointed the pivotal role of residues K303 and E488 in the activation cascade of I290M. This insight was substantiated by biophysical assays, as disruption of the K303-E488 interaction curtailed the thermal stabilization characteristic of the I290M mutation. These findings designate K303 and E488 as potential targets for inhibitors aimed at modulating PPARγ activation, with promising implications for refining bladder cancer prognosis. In sum, our study highlights the remarkable predictive capabilities achieved through the integration of simulation and cheminformatics methods, validated by biochemical experiments, to gain deeper insights into molecular mechanisms of activation and identify target residues for protein modulation.</p>
Effects of CYP2E1, CYP1A1 and CYP1A2 polymorphisms influence on bladder cancer
<p><span>The polymorphisms of <em>CYP2E1</em> (rs2515641), <em>CYP1A1 </em>(rs4646422), <em>CYP1A2 </em>(rs762551 and rs2470890) were genotyped in <a name="_Hlk122091441"></a>217 bladder cancer patients and <a name="_Hlk122091454"></a>550 healthy controls using t</span><span>he Agena MassARRAY system</span><span>.</span></p>
Supplemental Data for Comprehensive Microbiome Landscape (Bladder, Intestinal, Vaginal) in Bladder Cancer: A Systematic Review
<p>Supplemental Data for: "<em>Comprehensive Microbiome Landscape (Bladder, Intestinal, Vaginal) in Bladder Cancer: A Systematic Review"</em></p>
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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.