Similar Datasets
Project description:We report areas of H3K27ac modification in both wild-type (parental) UMUC-1 and UMUC-1 FOXA1 KO bladder cancer cells.
2022-09-08 | GSE172432 | GEO
Project description:We report areas of H3K27ac modification in both wild-type (parental) UMUC-1 and UMUC-1 FOXA1 KO bladder cancer cells.
2022-09-08 | GSE172431 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-09-08 | GSE172433 | GEO
Project description:Bladder cancer is common in elderly men, and it is a highly mutated tumor with frequent TP53 and FGFR3 mutation. Young-onset bladder cancer (YBC) is extremely rare; therefore, its genomic characteristics are unknown and appropriate management strategy is yet to be defined. Through a nation-wide search for bladder cancer diagnosed at 20 years or younger, 29 cases of biopsy-proven YBCs were collected. Whole exome sequencing and RNA sequencing were performed on 21 and 11 cases, respectively, and the results were compared with those of adult bladder cancer (ABC) retrieved from public database. Almost all YBCs were low grade, non-invasive papillary tumors. YBC had low mutation burden and less complex copy number alterations. Driver mutations were found in all cases. Common mutations included HRAS mutations (10 cases) with a preference in exon 5 and FGFR3 gene fusions (7 cases) with various partner genes, which occurred in a mutually exclusive manner. Other alterations included KRAS mutations (2 cases), arm-level deletion of chromosomes 4p and 10q (1 case), and ERCC2 mutation (1 case). TP53 and FGFR3 point mutations were not found. The gene expression profiles of YBC corresponded to those of the good prognostic group of ABC. No YBC cases had progressed to muscle-invasive tumor during follow-up. In addition, ABCs with YBC-like mutations also showed no progression to muscle-invasive tumor. In conclusion, YBC had distinct driver genetic alterations such as HRAS mutation and FGFR3 gene fusion and showed good prognosis. YBCs and ABCs with YBC-like mutations may be managed with less aggressive surveillance.
2020-03-30 | GSE133192 | GEO
Project description:Urothelial cell carcinoma of the bladder (UCC) is a common disease characterized by FGFR3 mutation. Whilst upregulation of this oncogene occurs most frequently in low-grade non-invasive tumors, recent data reveal increased FGFR3 expression characterizes a common sub-type of invasive UCC sharing genetic similarities with lobular breast cancer. These similarities include upregulation of the FOXA1 transcription factor and reduced expression of microRNAs-99a/100. We have previously identified direct regulation of FGFR3 by these two microRNAs and now search for further targets. Using a microarray meta-database we find potential FOXA1 regulation by microRNAs-99a/100. We confirm direct targeting of the FOXA1 3âUTR by microRNAs-99a/100 and also potential indirect regulation through microRNA-485-5p/SOX5/JUN-D/FOXL1 and microRNA-486/FOXO1a. In 292 benign and malignant urothelial samples, we find an inverse correlation between the expression of FOXA1 and microRNAs-99a/100 (r=-0.33 to -0.43, p<0.05). As for FGFR3 in UCC, tumors with high FOXA1 expression have lower rates of progression than those with low expression (Log rank p=0.009). Using global gene expression and CpG methylation profiling we find genotypic consequences of FOXA1 upregulation in UCC. These are associated with regional hypomethylation and near FOXA1 binding sites, and mirror patterns previously reported in FGFR3 mutant UCC. These include gene silencing through aberrant hypermethylation (e.g. IGFBP3) and affect genes that characterize lobular breast cancer (e.g. ERBB2, XBP1). In conclusion, we have identified microRNAs-99a/100 mediate a direct relationship between FGFR3 and FOXA1, and potentially facilitate cross talk between these pathways in UCC. Gene expression profiling of EJ Bladder cancer cells transfected with FOXA1 construct or with empty pUC19 vector.
2014-08-01 | E-GEOD-56037 | biostudies-arrayexpress
Project description:Recent findings suggested a benefit of anti-EGFR therapy for basal-like muscle invasive bladder cancer (MIBC). However, impact on bladder cancer with substantial squamous differentiated (Sq-BLCA) and especially pure squamous cell carcinoma (SCC) remains unknown. Therefore, we comprehensively characterized pure and mixed Sq-BLCA (n=125) on genetic and protein expression level, and performed functional pathway and drug-response analyses with cell line models and isolated primary SCC (p-SCC) cells of the human urinary bladder. We identified abundant EGFR expression in 95% of Sq-BLCA without evidence for activating EGFR mutations. Both SCaBER and p-SCC cells were sensitive to EGFR tyrosine kinase inhibitors (TKIs: erlotinib and gefitinib). Combined treatment with anti-EGFR TKIs and varying chemotherapeutics led to a concentration-dependent synergism in SCC cells according to the Chou-Talalay method. In addition, siRNA knockdown of EGFR impaired SCaBER viability suggesting a putative ‘‘Achilles heel’’ of Sq-BLCA. The observed effects seem Sq-BLCA-specific since non-basal urothelial cancer cells were characterized by poor TKI sensitivity associated with a short-term feedback response by upregulating EGFR and ERBB3 expression. Hence, our findings give novel insights into a crucial, Sq-BLCA-specific role of the ERBB signaling pathway proposing improved effectiveness of combined anti-EGFR and chemotherapeutic regimens in squamous bladder cancers with wild-type EGFR-overexpression.
2023-03-12 | GSE146975 | GEO
Project description:Interstitial cystitis (IC) and bladder pain syndrome are terms used to describe a heterogenous chronic pelvic and bladder pain disorder of unknown etiology. The goal of this pilot study was to determine if gene expression profiling of bladder biopsy tissue from patients experiencing symptoms could be used to separate the patients based on some clinical parameter. Gene expression profiles in bladder biopsy tissue from patients with: (1) low bladder capacity (defined here as <400 ml upon hydordistension), (2) normal capacity (M-bM-^IM-%400 ml), and (3) controls were compared. Gene expression profiles from low bladder capacity tissues differed significantly from normal capacity and control tissue, suggesting gene expression profiling may be a useful tool for better understanding IC disease pathophysiology.
2014-05-13 | E-GEOD-57560 | biostudies-arrayexpress
Project description:Urogenital schistosomiasis (caused by Schistosoma haematobium) remains a major public health concern worldwide. In response to parasite egg deposition, the host bladder undergoes gross and molecular morphological changes relevant for disease manifestation. However, limited mechanistic studies to date imply that the molecular mechanisms underlying pathology have not been well-defined. We leveraged a mouse model of urogenital schistosomiasis to perform for the first time, proteome profiling of the early molecular events that occur in the bladder after exposure to S. haematobium eggs, and to elucidate the protein pathways involved in urogenital schistosomiasis-induced pathology. Purified S. haematobium eggs or control vehicle were microinjected into the bladder walls of mice. Mice were sacrificed seven days post-injection and bladder proteins isolated and processed for proteome profiling using mass spectrometry.
2022-01-23 | PXD029852 | Pride
Project description:Rat bladder cancer cells (AY-27 cell line) were inoculated intravesically into syngeneic female Fischer rats. The bladder was analyzed by histology and Affymetrix GeneChips and compared to bladders from sham operated and normal rats.
2009-04-22 | E-MTAB-104 | biostudies-arrayexpress
Project description:To investigate whether the bladder assembloids recapitulate cell compositions, in addition to the gene expression patterns of each cell type in the adult bladder, we performed single-cell RNA-seq of bladder assembloids and mouse adult bladders, and compared the transcriptional profiles between them at the single-cell level.
2020-09-27 | GSE141348 | GEO