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Links from GEO DataSets

Items: 18

1.

Expression data of PTEN deficient PKO cells

(Submitter supplied) Incurable metastatic castration-resistant prostate cancer (CRPC) eventually occurs after androgen deprivation treatment. It is important to understand how CRPC initiates/progress. We generated a mouse androgen-independent prostate cancer cell line (PKO) from PTEN null and Hi-Myc transgenic mice in C57BL/6 background. Here we analyzed the expression profiles of PKO cells.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
7 Samples
Download data: CEL
Series
Accession:
GSE233306
ID:
200233306
2.

Genome-wide Profiling of SRC-2 (NCOA2) binding in mouse prostate [ChIP-Seq]

(Submitter supplied) Using genetically engineered mice, overexpressing SRC-2, specifically in the prostate epithelium of PTEN heterozygous mice accelerates PTEN mutation induce tumor progression and develops a metastasis-prone cancer. Here we used ChIP-Seq analysis to identify genome-wide SRC-2 binding sites in mouse prostate.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
2 Samples
Download data: BW
Series
Accession:
GSE54770
ID:
200054770
3.

A pivotal role of SRC-2 in Metastatic and Castration Resistant Prostate Cancer

(Submitter supplied) SRC-2 is frequently amplified or overexpressed in metastatic prostate cancer patients. In this study, we used genetically engineered mice, overexpressing SRC-2 specifically in the prostate epithelium as a mouse model to examine the role of SRC-2 in prostate tumorigenesis. Over-expression of SRC-2 in PTEN heterozygous mice accelerates PTEN mutation induced tumor progression and develops a metastasis-prone cancer. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE54678
ID:
200054678
4.

PB-Cre/Pten/Smad4 mouse prostate cancer micorarray for CRPC and lung metastasis studies

(Submitter supplied) PB-Cre/Pten/Smad4 is a transgenic mouse model of metastatic prostate adenocarcinoma (PMID: 21289624). To study the transcriptomic alterations associated with castration-resistant prostate cancer (CRPC), the PB-Cre/Pten/Smad4 males with established prostate cancer were treated with surgical castration followed by enzalutamide-admixed diet. After about 4 weeks, dorsolateral prostate (DLP) lobes of treatment-naïve prostate tumors (N=2) and CRPC tumors (N=3) were harvested and extracted for RNA purification and microarray profiling. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
9 Samples
Download data: CEL
Series
Accession:
GSE163420
ID:
200163420
5.

High fidelity patient-derived xenografts for accelerating prostate cancer discovery and drug development

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome variation profiling by genome tiling array
Platforms:
GPL14550 GPL10123 GPL10152
56 Samples
Download data: TXT
Series
Accession:
GSE41193
ID:
200041193
6.

HDAC inhibition impedes epithelial–mesenchymal plasticity and suppresses metastatic, castration-resistant prostate cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing
Platforms:
GPL10361 GPL13112
17 Samples
Download data: TXT
Series
Accession:
GSE67879
ID:
200067879
7.

HDAC inhibition impedes epithelial–mesenchymal plasticity and suppresses metastatic, castration-resistant prostate cancer

(Submitter supplied) PI3K (phosphoinositide 3-kinase)/AKT and RAS/MAPK (mitogen-activated protein kinase) pathway coactivation in the prostate epithelium promotes both epithelial–mesenchymal transition (EMT) and metastatic castration-resistant prostate cancer (mCRPC), which is currently incurable. To study the dynamic regulation of the EMT process, we developed novel genetically defined cellular and in vivo model systems from which epithelial, EMT and mesenchymal-like tumor cells with Pten deletion and Kras activation can be isolated. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10361
11 Samples
Download data: TXT
Series
Accession:
GSE67872
ID:
200067872
8.

HDAC inhibition impedes epithelial–mesenchymal plasticity and suppresses metastatic, castration-resistant prostate cancer

(Submitter supplied) PI3K (phosphoinositide 3-kinase)/AKT and RAS/MAPK (mitogen-activated protein kinase) pathway coactivation in the prostate epithelium promotes both epithelial–mesenchymal transition (EMT) and metastatic castration-resistant prostate cancer (mCRPC), which is currently incurable. To study the dynamic regulation of the EMT process, we developed novel genetically defined cellular and in vivo model systems from which epithelial, EMT and mesenchymal-like tumor cells with Pten deletion and Kras activation can be isolated. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE67681
ID:
200067681
9.

HIF1a inhibition overcomes castration resistance

(Submitter supplied) We used single-cell RNA sequencing to understand castration resistance in a murine model of prostate cancer
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21626
2 Samples
Download data: MTX, TSV
Series
Accession:
GSE216158
ID:
200216158
10.

Newly developed preclinical models reveal broad spectrum CDK inhibitors as potent drugs for CRPC exhibiting primary resistance to enzalutamide

(Submitter supplied) Androgen-deprivation therapy is a standard treatment for advanced prostate cancer. However, most patients eventually acquire resistance and progress to castration-resistant prostate cancer (CRPC). In this study, we established new CRPC cell lines, AILNCaP14 and AILNCaP15, from LNCaP cells under androgen-deprived conditions. Unlike most pre-existing CRPC cell lines, both cell lines expressed higher levels of androgen receptor (AR) and prostate-specific antigen (PSA) than parental LNCaP cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
24 Samples
Download data: XLSX
Series
Accession:
GSE258991
ID:
200258991
11.

Targeting the fibroblast growth factor pathway in molecular subtypes of castration-resistant prostate cancer

(Submitter supplied) Androgen receptor (AR) pathway inhibition remains the cornerstone for first- and second-line prostate cancer therapies. Although AR signaling inhibitors, such as enzalutamide and abiraterone extend survival in recurrent and castration-resistant prostate cancer (CRPC), durable and complete responses are rare. Resistance mechanisms employed by metastatic CRPC include amplification of AR and AR splice variants in AR-positive CRPC (ARPC) and conversion to AR-null phenotypes, such as double-negative prostate cancer (DNPC) and small cell or neuroendocrine prostate cancer (SCNPC). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL16791
194 Samples
Download data: TXT
Series
Accession:
GSE228283
ID:
200228283
12.

AR-V7 Targets in Castration-Resistant Prostate Cancer (CRPC) Cell Line

(Submitter supplied) In order to define the genes responsible for the growth and survival of a human castration-resistant prostate cancer cell line, a short term (doxycycline inducible) knockdown system was developed and utilized. Three independent 22Rv1 cell isolates were derived for each of the following doxycycline-inducible shRNAs (shGFP, shAR3, and shVav3) (AR3 = AR-V7). The cells were grown in androgen depleted conditions, plus or minus doxycycline, for three days. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
18 Samples
Download data: CEL
Series
Accession:
GSE104572
ID:
200104572
13.

Transcriptome analysis of VCaP xenografts resistant to dual therapy with abiraterone and enzalutamide

(Submitter supplied) We report RNA sequencing data on serial biopsies of prostate cancer VCaP xenografts as the tumors pass from androgen-sensitivity (Pre-Cx), to castration resistance (CRPC, castration resistant prostate cancer), onto resistance to dual therapy with abiraterone plus enzalutamide (AER). From comparison of these RNAseq data sets, we were able to determine differentially expressed genes between the AER/CRPC and Pre-Cx states that could mediate resistance to androgen deprivation therapies.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: TXT
14.

A constitutively activated form of the p110 beta isoform of PI3-kinase induces prostatic intraepithelial neoplasia in mice

(Submitter supplied) The global gene expression profiles of ventral prostates of wild type mice and p110 beta transgenic mice.
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4108
Platform:
GPL8321
8 Samples
Download data: CEL
Series
Accession:
GSE21543
ID:
200021543
15.
Full record GDS4108

Prostate response to activated form of p110β isoform of PI3-kinase

Analysis of ventral prostate from transgenics expressing a constitutively activated p110β allele in prostate. Activation of the p110β isoform causes mouse prostatic intraepithelial neoplasia (mPIN). Results provide insight into ability of an activated allele of p110β to induce prostatic tumor.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 2 disease state sets
Platform:
GPL8321
Series:
GSE21543
8 Samples
Download data: CEL
16.

Transcriptomic analysis of the in vivo effects of CDK8/19 inactivation in 22Rv1 xenografts growing in intact and castrated NSG mice

(Submitter supplied) RNA-Seq analysis was carried out to investigate the effects of CDK8/19 inactivation in the tumors formed in intact and castrated NSG mice by different 22Rv1 derivatives, with or without SNX631 treatment. The 22Rv1 derivatives were generated as following: Parental 22Rv1 (Rv1-WT) were transduced with a lentivirus expressing luciferase, yielding the derivative Rv1-Luc. 22Rv1 cells with a double knockout of CDK8 and CDK19 (Rv1-dKO) were made via CRISPR/Cas9. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL20301 GPL24676
66 Samples
Download data: TXT
Series
Accession:
GSE240370
ID:
200240370
17.

Effects of CDK8/19 Mediator Kinase inhibition on gene expression in castration-resistant prostate cancer cell line 22Rv1 and its derivatives grown in vitro.

(Submitter supplied) RNA-Seq analysis was carried out to investigate the effects of selective CDK8/19 inhibitor SNX631 on gene expression in different 22RV1 derivatives grown in cell culture, under androgen-supplemented and androgen-deprived conditions. The 22Rv1 derivatives were generated as following: Parental 22Rv1 (Rv1-WT) were transduced with a lentivirus expressing luciferase, yielding the derivative Rv1-Luc. 22Rv1 cells with a double knockout of CDK8 and CDK19 (Rv1-dKO) were made via CRISPR/Cas9. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL20301
48 Samples
Download data: TXT
Series
Accession:
GSE240369
ID:
200240369
18.

Effects of CDK8/19 Mediator Kinase inhibition by Senexin B and SNX631 on androgen-regulated gene expression in LNCaP cells

(Submitter supplied) RNA-Seq analysis was carried out to investigate the effects of selective CDK8/19 inhibitor Senexin B and SNX631 on gene expression in LNCaP prostate cancer cells treated with or without androgen.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
28 Samples
Download data: TXT
Series
Accession:
GSE240167
ID:
200240167
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