Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260065 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1562850_1.fastq.gz | Fastqsanger.gz | |||
| SRR1562850_2.fastq.gz | Fastqsanger.gz | |||
| SRR1562847_1.fastq.gz | Fastqsanger.gz | |||
| SRR1562847_2.fastq.gz | Fastqsanger.gz | |||
| SRR1562848_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:A transgenic TMPRSS2:ERG mouse model was engineered in FVB background and compared to its wildtype counterpart in the absence of any treatment This experiment is designed to look at ERG-dependent changes in phenotype and gene expression
2014-09-03 | GSE61008 | GEO
Project description:Common epithelial cancers are believed to become more aggressive through the accumulation of multiple independent molecular events that lead to the deregulation of cell signaling. However, the discovery that the majority of prostate cancers harbor gene fusions of the 5'-untranslated region of androgen regulated TMPRSS2 promoter with ETS transcription factor family members has brought this paradigm into question1,2. TMPRSS2-ERG gene fusion is the most common molecular sub-type of prostate cancer. Recent work suggests that the TMPRSS2-ERG fusion is associated with a more aggressive clinical phenotype3. In the most advanced castration resistant prostate cancers where the androgen receptor has been inactivated, the TMPRSS2-ERG fusion remains functionally active. Here we show compelling clinical and gene expression data supporting the existence of a TMPRSS2-ERG fusion prostate cancer subclass. Using expression array profiling on 455 primary prostate tumors, we identified an 87 gene expression signature, distinguishing TMPRSS2-ERG fusion prostate cancer as a discrete molecular entity. Computational analysis suggested that this fusion signature was associated with estrogen receptor signaling. Functional studies demonstrated regulation of the TMPRSS2-ERG fusion transcript by estrogenic compounds. These data identify a previously unrecognized mechanism for regulation of the TMPRSS2-ERG, even in the absence of a functional androgen receptor, and thus may have broader implications in the treatment of prostate cancer. Keywords: Prostate cancer, Expression array, Illumina, gene fusion, TMPRSS2, ERG, Signatures, Estrogen Test Cohort: 388 cases from the population based Swedish-Watchful Waiting cohort. The cohort consists of men with localized prostate cancer (clinical stage T1-T2, Mx, N0); Validation cohort: The PhysiciansM-bM-^@M-^Y Health Study (PHS) cohort included 116 US men diagnosed with incidental prostate cancer between 1983 and 2003; 455 cases were annotated for TMPRSS2-ERG fusion. Test Set: GSM208029 ... GSM208392 Validation Set: GSM208404 ... GSM208512
2008-05-27 | E-GEOD-8402 | biostudies-arrayexpress
Project description:Common epithelial cancers are believed to become more aggressive through the accumulation of multiple independent molecular events that lead to the deregulation of cell signaling. However, the discovery that the majority of prostate cancers harbor gene fusions of the 5'-untranslated region of androgen regulated TMPRSS2 promoter with ETS transcription factor family members has brought this paradigm into question1,2. TMPRSS2-ERG gene fusion is the most common molecular sub-type of prostate cancer. Recent work suggests that the TMPRSS2-ERG fusion is associated with a more aggressive clinical phenotype3. In the most advanced castration resistant prostate cancers where the androgen receptor has been inactivated, the TMPRSS2-ERG fusion remains functionally active. Here we show compelling clinical and gene expression data supporting the existence of a TMPRSS2-ERG fusion prostate cancer subclass. Using expression array profiling on 455 primary prostate tumors, we identified an 87 gene expression signature, distinguishing TMPRSS2-ERG fusion prostate cancer as a discrete molecular entity. Computational analysis suggested that this fusion signature was associated with estrogen receptor signaling. Functional studies demonstrated regulation of the TMPRSS2-ERG fusion transcript by estrogenic compounds. These data identify a previously unrecognized mechanism for regulation of the TMPRSS2-ERG, even in the absence of a functional androgen receptor, and thus may have broader implications in the treatment of prostate cancer. Keywords: Prostate cancer, Expression array, Illumina, gene fusion, TMPRSS2, ERG, Signatures, Estrogen
2008-05-28 | GSE8402 | GEO
Project description:ERG is a transcriptional factor, which is recombined with promoter of TMPRSS2 and prominently overexpressed in half of human prostate cancers. The mechanisms of ERG-mediated oncogenesis are not completely understood. We performed an unbiased Mass Spectrometry screen for ERG-binding proteins and found that ERG binds to MTDH/SND1 protein complex in prostate cancer cells. We determined that ERG binds to the SND1/MTDH protein complex via SND1 and this interaction plays a critical role in ERG-mediated cancer.
2023-03-22 | PXD036882 | Pride
Project description:A transgenic TMPRSS2:ERG mouse model was engineered in FVB background and compared to its wildtype counterpart in the absence of any treatment This experiment is designed to look at ERG-dependent changes in phenotype and gene expression A loxP-GFP-loxP-hERG exon 4-11 cassette was inserted into a BAC clone containing the TMPRSS2 locus using a recombineering kit. This modified BAC was used for pronuclear injection and generation of germline-transmitting mice. One line expressing high GFP was used for pronuclear injection of Cre protein and one sub-line that transmitted the TMPRSS2:ERG transgene into the germline was subsequently bred to homozygosity.
2014-09-03 | E-GEOD-61008 | biostudies-arrayexpress
Project description:Antineoplastic effects of siRNA against TMPRSS2-ERG junction oncogene in prostate cancer: from molecular and cellular studies to preclinical investigations. Background of the study.:TMPRSS2-ERG junction oncogene is present in more than 50% of patients with prostate cancer, and its expression is frequently associated with poor prognosis. We knockdown by siRNA the two TMPRSS2-ERG fusion variants (III and IV) most frequently identified in patients’ biopsies and found an inhibition of TMPRSS2-ERG of above 70% in human prostate cancer VCaP cell line expressing TMPRSS2-ERG junction oncogene. To point out genes regulated after TMPRSS2-ERG oncogene silencing, microarray analysis was performed.. Materiel and Methods. Human prostate cancer VCaP cell line expressing TMPRSS2-ERG oncogene (ATCC® CRL-2876™ Manassas, USA) was grown in Dulbecco's Modified Eagle Medium (DMEM) (Invitrogen, Cergy-Pontoise, France) supplemented with 10% fetal bovine serum (FBS), 100 units/ml penicillin and 100 μg/ml streptomycin (Invitrogen). Cells were incubated at 37°C in a humidified atmosphere containing 5% CO2. Transfection was carried out using Lipofectamine RNAiMAX transfecting agent (Invitrogen) according to manufacturer's instructions. Briefly, 8×105 VCaP cells were seeded in six-well plates in DMEM supplemented with 10% FCS, penicillin (100U/ml) and streptomycin (10µg/ml) and transfected with 50 nM siRNA TMPRSS2-ERG III, siRNA TMPRSS2-ERG IV and siRNA Control and 6 μL Lipofectamine® RNAiMAX. Cells were incubated with siRNA for 48h. At the end of the treatments, total RNAs of untreated cells (NT) and transfected cells were extracted using RNeasy mini-kit (Quiagen, Courtaboeuf, France). Three independent experiments were performed. Results. Microarray analysis confirmed ERG inhibition by both siRNA TMPRSS2-ERG III and IV and revealed a common down-regulated gene, ADRA2A, involved in cell proliferation and migration. Experiments are performed with Agilent Whole Genome 8x60K (028004) microarray. In triplicate with a non treated control cells, a control with ascramble siRNA, a siRNA TMPRSS2-ERG III, a siRNA TMPRSS2 IV.
2015-01-09 | E-MTAB-2838 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE28948: TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (gene expression data) GSE28950: TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (ChIP-Seq data) GSE35540: TMPRSS2-ERG, HDACs and EZH2 are involved in an AR centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (gene expression after ERG KD) Refer to individual Series
2012-04-26 | E-GEOD-28951 | biostudies-arrayexpress
Project description:Here, we developed immunoprecipitation-mass spectrometry assays for the measurement of a low-abundance T1E4 TMPRSS2-ERG fusion protein, its isoforms and its interactome in VCaP prostate cancer cells.
2021-03-29 | PXD021236 | Pride
Project description:Prostate tumors with the gene fusion TMPRSS2:ERG have been reported to have a significantly higher risk of recurrence compared with tumors lacking the fusion. Tumors from 139 patients who underwent radical prostatectomy were analyzed for the expression of 502 cancer-related genes to identify genes differentially regulated in TMPRSS2:ERG fusion tumors as well as identify biomarkers of biochemical recurrence. 139 prostate fresh-frozen tumors from radical prostatectomy surgery where profiled on the Illumina Human Cancer DASL Panel. 69 tumors were positive for the gene fusion TMPRSS2:ERG while 70 where not. 33 of the 139 patients experienced biochemical recurrence. Data was analyzed for differential genes in TMPRSS2:ERG fusion positive tumors as well as clinical and molecular biomarkers of recurrence.
2009-10-22 | E-GEOD-18655 | biostudies-arrayexpress
Project description:Prostate cancer is the second most common cancer among men worldwide. Alterations in the DNA methylation pattern can be one of the leading causes for prostate cancer formation. This study is the first high throughput sequencing study investigating genome-wide DNA methylation patterns in a large cohort of 51 tumor and 53 benign prostate samples using MeDIP-Seq. Comparative analyses identified more than 147,000 cancer-associated epigenetic alterations. Additionally, global methylation patterns demonstrate significant differences based on the TMPRSS2:ERG rearrangement status. We propose the hypermethylation of miRNA-26a as an alternative pathway of ERG rearrangement independent EZH2 activation. The observed increase in differential methylation events in fusion negative tumors can explain the tumorigenic process in the absence of genomic rearrangements. Genomewide examination of methylation profiles in 51 prostate cancer samples
2012-12-06 | E-GEOD-35342 | biostudies-arrayexpress