GEO DataSets

Analysis of bladder cancer cell line RT112 subjected to doxycycline-inducible, shRNA knockdown of FGFR3. Knockdown of FGFR3 in RT112 cells significantly attenuates tumor growth in vitro and in vivo. Results provide insight into the molecular mechanisms underlying FGFR3-driven bladder cancer.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 4 genotype/variation, 2 protocol sets

Platform:

GPL570

Series:

GSE41035

24 Samples

Download data: CEL

(Submitter supplied) Aberrant activation of FGFR3 via overexpression or mutation is a frequent feature of bladder cancer; however, its molecular and cellular consequences and functional relevance to carcinogenesis are not well understood. In this study with a bladder carcinoma cell line expressing inducible FGFR3 shRNAs, we sought to identiy transcriptional targets of FGFR3 and investigate their contribution to bladder cancer development.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4454

Platform:

GPL570

24 Samples

Download data: CEL

(Submitter supplied) To address the molecular mechanisms underlying c-Src-mediated tumor progression, we previously developed a model system using Csk-deficient fibroblasts that can be transformed by wild-type c-Src. In this study, we applied this system for the analysis of the potential contribution of miRNA to c-Src-mediated transformation. Pair-wise significance analysis of the microarray indicated that seven miR genes were significantly upregulated and six miRNA genes were downregulated in c-Src-transformed cells with a P value below 0.01 and with a fold change over 2.0.

Organism:

Mus musculus

Type:

Non-coding RNA profiling by array

Platform:

GPL9756

8 Samples

Download data: TXT

(Submitter supplied) Presently, there is a deficiency of effective therapies designed to target clear cell renal cell carcinoma (ccRCC), with poor prognosis resulting in patients with advanced disease. Additionally, there is a lack of molecular factors which can be remedially targeted resulting in tumor specific inhibition, and therefore current therapeutic approaches often produce adverse side effects in patients. We identified that Stearoyl-CoA desaturase 1 (SCD1) was consistently overexpressed in patient ccRCC samples, and further investigation of SCD1 as a potential molecular target for ccRCC intervention utilizing a SCD1 inhibitor (A939572) resulted in tumor specific growth inhibition and induction of cell death. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS5094

Platform:

GPL570

8 Samples

Download data: CEL

Analysis of clear cell renal cell carcinoma (ccRCC) cells treated with A939572, a stearoyl-CoA desaturase 1 (SCD1) inhibitor. SCD1 is overexpressed in ccRCC.Results provide insight into the role of SCD1 in the pathogenesis of ccRCC.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 agent, 4 cell line sets

Platform:

GPL570

Series:

GSE41485

8 Samples

Download data: CEL

(Submitter supplied) Currently there is a lack of effective therapies which result in long-term durable response for patients presenting with anaplastic thyroid carcinoma (ATC), a very rare and lethal variant of thyroid cancer. ATC is resistant to chemotherapy, radiation, and targeted therapies currently available. In an effort to identify novel tumor-specific therapeutic targets, we performed high throughput gene array analysis screening numerous patient ATC tumor tissues, and compared their gene expression levels to matched and unmatched normal thyroid tissue samples.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

25 Samples

Download data: CEL

(Submitter supplied) We hypothesized that ETV5 may be a mediator of the oncogenic effects of mutant FGFR3 in bladder cancer cells ETV5 was silenced by shRNA in the bladder cancer cell line 97-7 to investigate effect on phenotype. To identify downstream gene targets of ETV5 we compared gene expression profiles in silenced and control cells.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

12 Samples

Download data: CEL

(Submitter supplied) The NFκB transcription factor is constitutively active in a number of hematologic and solid tumors, and many signaling pathways implicated in cancer are likely connected to NFκB activation. A critical mediator of NFκB activity is TGFβ-activated kinase 1 (TAK1). Here, we identify TAK1 as a novel interacting protein and direct target of fibroblast growth factor receptor 3 (FGFR3) tyrosine kinase activity. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS5023

Platform:

GPL6244

12 Samples

Download data: CEL

Analysis of fibroblast growth factor receptor 3 (FGFR3)-positive, MGHU3 (Y375C) bladder cancer cells depleted for TGFβ-activated kinase 1 (TAK1) then treated with FGFR-specific PD173074 inhibitor. Results provide insight into the integration of TAK1 and FGFR3 signaling in bladder cancer.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 agent, 2 genotype/variation sets

Platform:

GPL6244

Series:

GSE52452

12 Samples

Download data: CEL

(Submitter supplied) Activating mutations of FGFR3 are found in a high proportion of bladder tumours. The molecular consequences of FGFR3 mutation in urothelial cells and the mechanisms by which mutant FGFR3 may drive bladder tumourigenesis are largely unknown. We used expression arrays to identify downstream targets of mutant FGFR3 signalling in normal urothelial cells.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

6 Samples

Download data: CEL

(Submitter supplied) To determine whether a TP63/KLF5-regulated super-enhancer region can impact SREBF1 transcription, circularized chromosome conformation capture (4C) assays were performed. 4C assays identified complex, extensive interactions between the SREBF1 promoter and the super-enhancer region Moreover, these DNA-DNA contacts were strictly confined within the super-enhancer region, highlighting the specificity of chromatin interactions

Organism:

Homo sapiens

Type:

Other

Platform:

GPL15520

2 Samples

Download data: TXT

(Submitter supplied) We profiled esophageal squamous cell carcinorma (ESCC) cell lines with chromatin immunoprecipitation sequencing (ChIP-Seq). Mathematically modeling was performed to establish (super)-enhancers landscapes and inter-connected transcriptional circuitry formed by master TFs. Coregulation and cooperation between master TFs was investigated by ChIP-Seq, RNASeq, 4C-Seq and luciferase assay. Biological functions of candidate factors were evaluated by measuring cell proliferation, colony formation, cell apoptosis and xenograft growth. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL22790 GPL10999

13 Samples

Download data: BW, NARROWPEAK, TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

54 Samples

Download data: BROADPEAK, BW, NARROWPEAK

(Submitter supplied) Bladder cancer prognosis is closely linked to the underlying differentiation state of the tumor, ranging from the less aggressive and most differentiated luminal tumors to the more aggressive and least differentiated basal tumors. Sequencing of bladder cancer has revealed that loss-of-function mutations in chromatin regulators and mutations that activate receptor tyrosine kinase (RTK) signaling frequently occur in bladder cancer. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

24 Samples

Download data: BROADPEAK, BW, NARROWPEAK

(Submitter supplied) Bladder cancer prognosis is closely linked to the underlying differentiation state of the tumor, ranging from the less aggressive and most differentiated luminal tumors to the more aggressive and least differentiated basal tumors. Sequencing of bladder cancer has revealed that loss-of-function mutations in chromatin regulators and mutations that activate receptor tyrosine kinase (RTK) signaling frequently occur in bladder cancer. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

30 Samples

Download data: CSV

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platforms:

GPL19109 GPL15236

11 Samples

Download data: CEL

(Submitter supplied) To better understand the molecular mechanisms underlying altered-FGFR3 oncogenic activity in bladder carcinomas, we made use of RT112 cell lines, which were derived from a human bladder tumor and endogenously expressed the FGFR3-TACC3 fusion protein, the growth and transformation of these cell lines being dependent on activated-FGFR3 activity. We conducted a gene expression analysis using Affymetrix DNA arrays in this cell line treated or not with FGFR3 siRNAs.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL19109

5 Samples

Download data: CEL

(Submitter supplied) To better understand the molecular mechanisms underlying altered-FGFR3 oncogenic activity in bladder carcinomas, we made use of MGH-U3 cell lines, which were derived from a human bladder tumor and endogenously expressed a mutated activated form of FGFR3 (FGFR3-Y375C), the growth and transformation of these cell lines being dependent on activated-FGFR3 activity. We conducted a gene expression analysis using Affymetrix DNA arrays in this cell line treated or not with FGFR3 siRNAs.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL15236

6 Samples

Download data: CEL

(Submitter supplied) 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.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL28635

15 Samples

Download data: CEL

(Submitter supplied) Metabolic reprogramming of bladder cancer cells driven by mutant FGFR3 increases serine synthesis that suppresses macrophage immunostimulatory functions to generate an immunosuppressive tumor microenvironment, which can be overcome by targeting PI3K.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

2 Samples

Download data: TAR