Gene expression profile of micropapillary bladder cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE86411 | GEO | 2016/09/03
SECONDARY ACCESSION(S): PRJNA341710
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptomic Analysis Of Micropapillary High Grade T1 Urothelial Bladder Cancer
| PRJNA562495 | ENA
Project description:Management of high-grade T1 (HGT1) micropapillary bladder cancer (MPBC) is controversial. An accurate genomic characterization might help predict outcome. We analyze the transcriptomic profile of MPBC in a clinically annotated HGT1 cohort establishing correlation with clinical outcome.A retrospective analysis of prospectively clinically followed series of HGT1; 23 patients with MPBC and 64 without MPBC (reference set). We identified a set of genes differentially expressed (DE). Associations between; clinical variables and gene expression (GE) levels (Wilcoxon’s rank sum); GE and time to progression (TTP) in univariate analysis (Log rank); GE levels adjusting for clinical variables (Cox regression) were evaluated.We identified a 26-gene signature that characterized MPBC in HGT1. Several genes including CD36, FAPB3 and RAETE1 were significantly associated with TTP. High expression of FABP3 and CD36 were associated with shorter TTP (P=0.045 and P=0.08 (NS)) as was low expression of RAET1E (P=0.01). Limitations include the lack of specific quantification of the percentage of MPBC tumor >10%.
2021-01-31 | GSE136401 | GEO
Project description:Micropapillary adenocarcinoma of the lung is a cancer with poor prognosis and characterized by the presence of tumor cells with ring-like glandular structure floating within alveolar spaces. We investigated the association between its morphological, biochemical, and immunohistochemical characteristics and malignancy using the KU-Lu-MPPt3 cell line established from a patient with micropapillary adenocarcinoma. Two subpopulations of KU-Lu-MPPt3 cells, adhesive (AD) and clumpy and suspended (CS) cells, were prepared and subjected to DNA microarray.
2021-09-28 | GSE184883 | GEO
Project description:Expression profiling by arrays Urothelial carcinoma (UC) can arise at any location along the urothelial tract, including the urethra, bladder, ureter or renal pelvis. Although tumors arising in these various locations demonstrate similar morphology, it is unclear whether the gene expression profiles are similar in the upper tract (ureter and renal pelvis) or in the lower tract (bladder and urethra) carcinomas, especially given their different embryologic origins. As differences may facilitate potentially different screening and treatment modalities, we sought to examine the relationship between urothelial carcinoma of the renal pelvis (rUC) and urothelial carcinoma of the bladder (bUC). Fresh tumor tissue was collected from patients with bUC (n=10) and benign mucosa from the bladder (n=7) was collected from individuals undergoing resection for non-UC conditions for comparison. Gene expression profiles from these samples were determined using high-throughput Affymetrix gene expression microarray chips. Bioinformatic approaches were used to compare gene expression profiles of these samples and those of rUC (n= 14) and normal kidney (n=14) that were mostly used in our previous publication. Using unsupervised analytic approaches, rUC and bUC were indistinguishable. When supervised analytic approach was used, a very small number of potentially differentially expressed genes was identified; these differences were most likely to be limited to a single pathway - the chloride ion binding activity pathway -which was more frequently activated in rUC than in bUC. We found that the gene expression profiles of UCs from the upper and lower tract were extremely similar, suggesting that similar pathogenic mechanisms likely function in the development of these tumors. The differential expression of genes in the identified pathway may represent a potential new avenue for detection of upper tract tumors. Tissue samples with urothelial cell carcinoma from lower tract (bladder) as well as normal references were collected and the gene expression profiles were compared with gene expression profiles of samples in our previously published data set . No technical replicates.
2010-12-31 | E-GEOD-24152 | biostudies-arrayexpress
Project description:Somatic mutations of the fibroblast growth factor receptor 3 (FGFR3) are one of the most frequent genetic alterations in bladder carcinomas. We report here that human-FGFR3-S249C expression in urothelial cells of transgenic mice induces low-grade papillary tumors presenting genomic instability and resembling human pTa urothelial tumors at the transcriptomic level. Mutated-FGFR3 expression levels impacted the incidence of tumor formation and could account for the tissue specificity of human mutated FGFR3-driven tumors restricted to epithelia presenting high normal expression levels of FGFR3.
2021-12-31 | GSE151888 | GEO
Project description:Expression profiling by arrays Urothelial carcinoma (UC) can arise at any location along the urothelial tract, including the urethra, bladder, ureter or renal pelvis. Although tumors arising in these various locations demonstrate similar morphology, it is unclear whether the gene expression profiles are similar in the upper tract (ureter and renal pelvis) or in the lower tract (bladder and urethra) carcinomas, especially given their different embryologic origins. As differences may facilitate potentially different screening and treatment modalities, we sought to examine the relationship between urothelial carcinoma of the renal pelvis (rUC) and urothelial carcinoma of the bladder (bUC). Fresh tumor tissue was collected from patients with bUC (n=10) and benign mucosa from the bladder (n=7) was collected from individuals undergoing resection for non-UC conditions for comparison. Gene expression profiles from these samples were determined using high-throughput Affymetrix gene expression microarray chips. Bioinformatic approaches were used to compare gene expression profiles of these samples and those of rUC (n= 14) and normal kidney (n=14) that were mostly used in our previous publication. Using unsupervised analytic approaches, rUC and bUC were indistinguishable. When supervised analytic approach was used, a very small number of potentially differentially expressed genes was identified; these differences were most likely to be limited to a single pathway - the chloride ion binding activity pathway -which was more frequently activated in rUC than in bUC. We found that the gene expression profiles of UCs from the upper and lower tract were extremely similar, suggesting that similar pathogenic mechanisms likely function in the development of these tumors. The differential expression of genes in the identified pathway may represent a potential new avenue for detection of upper tract tumors.
2010-12-31 | GSE24152 | GEO
Project description:Here we report the discovery of truncating mutations of the gene encoding the cohesin subunit STAG2, which regulates sister chromatid cohesion and segregation, in 36% of papillary non-invasive urothelial carcinomas and 16% of invasive urothelial carcinomas of the bladder. Our studies suggest that STAG2 has a role in controlling chromosome number but not the proliferation of bladder cancer cells. These findings identify STAG2 as one of the most commonly mutated genes in bladder cancer. Affymetrix CytoScan HD Arrays were performed according to the manufacturer's directions on genomic DNA extracted directly from 12 snap-frozen human urothelial carcinoma primary tumors with somatic mutations of the STAG2 gene.
2013-06-30 | GSE41581 | GEO
Project description:In this study we applied differential gene expression analysis to exfoliated human urothelia obtained from patients of known bladder disease status. Selected targets from the microarray data were validated in an independent set of samples using a quantitative PCR approach. Total RNA was extracted from 52 samples of human urothelial cancer cells (C) and from 40 samples of human non-cancer (NC) urothelial cells. Fragmented, biotinylated cRNA was hybridized to Affymetrix Human Genome U133 Plus 2.0 microarrays.
2013-01-08 | E-GEOD-31189 | biostudies-arrayexpress
Project description:Aneuploidy is among the most common hallmarks of cancer, yet the underlying genetic mechanisms are still poorly defined. We have recently identified STAG2 as a gene that is mutated in human cancer and whose inactivation leads directly to chromosomal instability and aneuploidy. However, no single tumor type has yet been identified in which inactivation of a cohesin subunit represents a predominant mutational event. Here we used immunohistochemistry to screen a panel of 2,214 tumors from each of the major human tumor types to identify additional tumor types harboring somatic loss of STAG2. Strikingly, STAG2 expression was completely absent in 18% of urothelial carcinomas, the most common type of bladder cancer and the fifth most common cancer in the United States. DNA sequencing revealed that somatic mutations of STAG2 were present in 21% of urothelial carcinomas, which were found to be a group of highly aneuploid tumors. The acquisition of STAG2 mutations was shown to be an early event in the pathogenesis of urothelial carcinoma. STAG2 loss was significantly associated with lymph node invasion, increased disease recurrence, and reduced cancer-specific survival. These results identify STAG2 as one of the most commonly mutated genes in bladder cancer discovered to date, and demonstrate that STAG2 inactivation defines an aggressive subtype of bladder cancer with particularly poor prognosis. Affymetrix CytoScan HD Arrays were performed according to the manufacturer's directions on genomic DNA extracted directly from snap-frozen human urothelial carcinoma primary tumors. Copy number analysis using Affymetrix CytoScan HD Arrays was performed for 12 human urothelial carcinomas of the bladder with truncating mutations of the STAG2 gene.
2013-06-30 | E-GEOD-41581 | biostudies-arrayexpress
Project description:We reported a comprehensive proteogenomics analysis, including whole-genome sequencing, RNA sequencing, and proteomics and phosphoproteomics profiling, of 448 trace-tumor-samples from 190 urothelial bladder neoplasm patients, covering the whole spectrum of disease stages and grades. DNA damage was a key signaling pathway in the progression of carcinoma in situ (CIS) and related to APOBEC signature. Proteogenomic integration analysis indicated the mutation of HRAS regulated mTOR signaling to form urothelial papilloma rather than papillary urothelial cancer (PUC). Glucolipid metabolism increase and lower immune cell infiltration were significantly associated with PUC compared to CIS. Proteomic analysis distinguished the origins of invasive tumors (PUC-derived and CIS-derived), related to distinct clinical prognosis and molecular features. Additionally, loss of RBPMS, associated with CIS-derived tumors, was validated to increase the activity of SMAD-bound JUN and promote metastasis.
2023-08-02 | PXD043775 | iProX