Waldman Bladder tumors
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE1827 | GEO | 2005/07/01
SECONDARY ACCESSION(S): PRJNA90395
REPOSITORIES: GEO
Similar Datasets
Project description:80 bladder tumors of different stages, grades and histologies analyzed on costom made cDNA arrays with 10638 gene elements
2010-06-09 | E-GEOD-1827 | biostudies-arrayexpress
Project description:To comprehensively understand the biological significance behind different grades of bladder cancer, we screened samples of different grades of bladder cancer and glandular cystitis from three patients for single-cell sequencing. In this study, We found that N-Glycan biosynthesis pathway was activated in high-grade bladder cancer while TNF-related pathway was activated in cystitis glandularis. More importantly, We discovered that N-Glycan biosynthesis is a potential target by cell assay and inhibition of this pathway may contribute to the treatment of bladder cancer.
2022-04-13 | GSE190888 | GEO
Project description:54 tumors of breast cancer; a random mix of histologies, stages, and grades. Keywords: other
2005-07-28 | GSE1477 | GEO
Project description:Background: Muscle-invasive bladder cancer is a common aggressive disease with unmet clinical needs. Recent work established a set of consensus bladder cancer transcriptomic subtypes that distinguishes the cell identity of bladder cancers for improved diagnosis and treatment. However, how these distinct subtypes are regulated remains unclear. Given the link between super-enhancers and the regulation of cell identity, we hypothesized that epigenetic activation of distinct super-enhancers could drive the transcriptional programs of the various bladder cancer subtypes. Results: Through integrated RNA sequencing and epigenomic profiling of histone marks (H3K27ac, H3K27me3, H3K9me3) in a diverse panel of 15 primary bladder tumours, seven bladder cancer cell lines, and two primary cultures from normal human urothelia, we established the first integrated epigenetic map of bladder cancer and demonstrate the link between bladder cancer subtype and epigenetic control. Through H3K27ac analysis, we identify the repertoire of activated super-enhancers in bladder cancer that distinguish molecular subtypes. Building on these findings, we reveal the super-enhancer-regulated networks of candidate master transcription factors for Luminal and Basal bladder cancer subgroups. We find that FOXA1, a key pioneer factor in Luminal bladder cancers identified in our Luminal transcription factor network, binds subgroup-specific bladder super-enhancers and correlates with their activation. Furthermore, CRISPR-Cas9 inactivating mutation of FOXA1 triggers a shift from Luminal to Basal cell identity. This shift is accompanied by an overexpression of ZBED2, one of the newly identified transcriptional regulators in the Basal-specific transcription factor network. 5Finally, we show that both FOXA1 and ZBED2 play concordant roles in preventing inflammatory response in bladder cancer cells through STAT2 inhibition and promote cancer cell survival. Conclusions: Overall, our study provides new data for understanding epigenetic regulation of muscle- invasive bladder cancer and identifies a coregulated network of super-enhancers and associated transcription factors as new potential targets for the treatment of this aggressive disease
2024-05-23 | GSE195768 | GEO
Project description:Using the highly sensitive lncRNA array, we screened the lncRNAs abundant in the human bladder cancer and Adjacent normal bladder tissues, and the function of differentially expressed lncRNAs were analyzed by bioinformatics. The Arraystar Human lncRNA Array (8x15K, Arraystar) and whole human mRNA Array (4x44K, Arraystar) and was used to profile differentially expressed lncRNAs and genes in bladder cancer vs. normal tissues following the manufacturerâs instructions. Briefly, extracted RNA template (1mg) was reversely transcribed into cDNA and digested into fragments with endonucleases. These fragments were labeled with DNA labeling reagent and labeled cDNAs were hybridized to the microarray via incubation at 45°C and rotated at 60 rpm for 17 h. Following washing and staining, the arrays were scanned using a GeneChip Scanner3000 with GeneChip Operating Software.
2016-07-02 | E-GEOD-83955 | biostudies-arrayexpress
Project description:miRNAs are involved in cancer development and progression,acting as tumor suppressors or oncogenes. Half of the human miRNAs are located in cancer-associated genomic regions and can function as tumor suppressor genes or oncogenes depending on their targets miRNA profiling was performed on paired bladder cancer tissues and differentially expressed miRNAs were identified in BC and adjacent noncancerous tissues of any disease stage/grade. Ten paired bladder cancer tissues (5 low-grade non-muscle-invasive bladder cancer[NMIBC] and 5 high-grade muscle-invasive bladder cancer[MIBC]) were sent to CapitalBio Corp. (Beijing) for noncoding RNA microarray analysis. The microarray analysis was done as described on the Web site of CapitalBio. NMIBC samples include 07A, 19A, 23A, 24A and T63 while coresponding pairs include 07B, 19B, 23B, 24B and 63. MIBC samples include 10A, 20A, 21A, 34A and 49A while coresponding pairs include 10B, 20B, 21B, 34B and 49B.
2012-07-06 | E-GEOD-39093 | biostudies-arrayexpress
Project description:This is a comprehensive genomic characterization of 40 urothelial bladder carcinoma (UBC) cell lines including information on origin, mutation status of genes implicated in bladder cancer (FGFR3, PIK3CA, TP53, and RAS), copy number alterations assessed using high density SNP arrays, uniparental disomy (UPD) events, and gene expression. Based on gene mutation patterns and genomic changes we identify lines representative of the FGFR3-driven tumor pathway and of the TP53/RB tumor suppressor-driven pathway. High-density array copy number analysis identified significant focal gains (1q32, 5p13.1-12, 7q11, and 7q33) and losses (i.e. 6p22.1) in regions altered in tumors but not previously described as affected in bladder cell lines. We also identify new evidence for frequent regions of UPD, often coinciding with regions reported to be lost in tumors. Previously undescribed chromosome X losses found in UBC lines also point to potential tumor suppressor genes. Cell lines representative of the FGFR3-driven pathway showed a lower number of UPD events. Overall, there is a predominance of more aggressive tumor subtypes among the cell lines. We provide a cell line classification that establishes their relatedness to the major molecularly-defined bladder tumor subtypes. The compiled information should serve as a useful reference to the bladder cancer research community and should help to select cell lines appropriate for the functional analysis of bladder cancer genes, for example those being identified through massive parallel sequencing. Expression levels were assessed in 20 bladder cell lines, included in the UBC-40 Urothelial Bladder Cell Line Index, with Affymetrix U133 array platform
2015-06-19 | E-GEOD-64279 | biostudies-arrayexpress
Project description:Background: Growing evidence has shown the association of long noncoding RNA/microRNA/mRNA is implicated in tumor initiation, development, and progression. Long noncoding RNA (lncRNA) HAND2-AS1 exhibits anti-cancer effects in diverse cancers. However, the knowledge of HAND-AS1 in bladder cancer remains largely unknown. The present study aims to investigate the effects and mechanisms of HAND-AS1 in bladder cancer progression. Methods: The expression of lncRNA was analyzed by RT2 lncRNA PCR Arrays. The differential expressed lncRNAs were further verified by qRT-PCR. The relationship between lncRNA expression and clinical features was evaluated with Spearman correlation test. Cell proliferation was measured by MTT assay. Cell apoptosis percentage was detected by ANNEXIN V-PI analysis. The promoter activity was illustrated by Luciferase assay, and the change of microRNA and protein was detected by qRT-PCR and western blot, separately. Results: The expression of HAND2-AS1 declined in bladder cancer and correlated with depth of invasion and grades negatively. Restoration of HAND2-AS1 hampered cell growth by provoking cell apoptosis. Furthermore, one of the HAND2-AS1 sponge, miR-146, was found overexpression in bladder cancer tissue and cell lines. Expression of miR-146 related to HAND2-AS1 expression negatively. One of the targeted genes of miR-146, retinoic acid receptor beta (RARB) was downregulated in bladder cancer. In addition, the expression of RARB related to miR-146 negatively. Lost-of-function and gain-of-function experiments were used to identify the mechanisms underlying association of lncRNA HAND2-AS1: miR-146: RARB. miR-146 targeted RARB directly and hindered RARB-mediate apoptosis. However, the hindrance was impaired by HAND2-AS1 notably. Conclusion: HAND2-AS1 diminished miR-146 expression, thereby releasing the suppression of miR-146 on RARB-mediated apoptosis, promoting bladder cancer regression.
2020-11-18 | GSE140585 | GEO
Project description:Background: Growing evidence has shown the association of long noncoding RNA/microRNA/mRNA is implicated in tumor initiation, development, and progression. Long noncoding RNA (lncRNA) HAND2-AS1 exhibits anti-cancer effects in diverse cancers. However, the knowledge of HAND-AS1 in bladder cancer remains largely unknown. The present study aims to investigate the effects and mechanisms of HAND-AS1 in bladder cancer progression. Methods: The expression of lncRNA was analyzed by RT2 lncRNA PCR Arrays. The differential expressed lncRNAs were further verified by qRT-PCR. The relationship between lncRNA expression and clinical features was evaluated with Spearman correlation test. Cell proliferation was measured by MTT assay. Cell apoptosis percentage was detected by ANNEXIN V-PI analysis. The promoter activity was illustrated by Luciferase assay, and the change of microRNA and protein was detected by qRT-PCR and western blot, separately. Results: The expression of HAND2-AS1 declined in bladder cancer and correlated with depth of invasion and grades negatively. Restoration of HAND2-AS1 hampered cell growth by provoking cell apoptosis. Furthermore, one of the HAND2-AS1 sponge, miR-146, was found overexpression in bladder cancer tissue and cell lines. Expression of miR-146 related to HAND2-AS1 expression negatively. One of the targeted genes of miR-146, retinoic acid receptor beta (RARB) was downregulated in bladder cancer. In addition, the expression of RARB related to miR-146 negatively. Lost-of-function and gain-of-function experiments were used to identify the mechanisms underlying association of lncRNA HAND2-AS1: miR-146: RARB. miR-146 targeted RARB directly and hindered RARB-mediate apoptosis. However, the hindrance was impaired by HAND2-AS1 notably. Conclusion: HAND2-AS1 diminished miR-146 expression, thereby releasing the suppression of miR-146 on RARB-mediated apoptosis, promoting bladder cancer regression.
2020-11-18 | GSE140584 | GEO
Project description:This is a comprehensive genomic characterization of 40 urothelial bladder carcinoma (UBC) cell lines including information on origin, mutation status of genes implicated in bladder cancer (FGFR3, PIK3CA, TP53, and RAS), copy number alterations assessed using high density SNP arrays, uniparental disomy (UPD) events, and gene expression. Based on gene mutation patterns and genomic changes we identify lines representative of the FGFR3-driven tumor pathway and of the TP53/RB tumor suppressor-driven pathway. High-density array copy number analysis identified significant focal gains (1q32, 5p13.1-12, 7q11, and 7q33) and losses (i.e. 6p22.1) in regions altered in tumors but not previously described as affected in bladder cell lines. We also identify new evidence for frequent regions of UPD, often coinciding with regions reported to be lost in tumors. Previously undescribed chromosome X losses found in UBC lines also point to potential tumor suppressor genes. Cell lines representative of the FGFR3-driven pathway showed a lower number of UPD events. Overall, there is a predominance of more aggressive tumor subtypes among the cell lines. We provide a cell line classification that establishes their relatedness to the major molecularly-defined bladder tumor subtypes. The compiled information should serve as a useful reference to the bladder cancer research community and should help to select cell lines appropriate for the functional analysis of bladder cancer genes, for example those being identified through massive parallel sequencing. Copy Number Variations were assessed in 45 bladder cell lines, included in the UBC-40 Urothelial Bladder Cell Line Index, with Human1M-Duov3 DNA Analysis BeadChip platform
2015-06-19 | E-GEOD-64572 | biostudies-arrayexpress