Ena-DATASET-IBT-12-06-2013-16:46:58:065-20 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001000610 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Whole transcriptome sequencing of 28 untreated prostate cancers, 13 castration resistant prostate cancers, and 12 benign prostatic hyperplasias.
| EGAD00001000609 | EGA
Project description:Small RNA sequencing of 28 untreated prostate cancers, 12 castration resistant prostate cancers, and 3 benign prostatic hyperplasias.
| EGAD00001000611 | EGA
Project description:Low coverage whole genome sequencing of 27 untreated prostate cancers, 9 castration resistant prostate cancers, and 4 benign prostatic hyperplasias.
| EGAD00001000612 | EGA
Project description:miRNA expression profiling of 13 clinical prostate samples, 4 benign prostate hyperplasias, 5 untreated primary prostate carcinomas and 4 castration-resistant prostate cancers.
2010-01-31 | E-MEXP-2319 | biostudies-arrayexpress
Project description:Androgens are a prequisite for the development of human prostate and prostate cancer. Androgen action is mediated via androgen receptor. Androgen ablation therapy is used for the treatment of metastasized prostate cancer. The aim of the study was to identify genes differentially expressed in benign human prostate, prostate cancer and in prostate tissue three days after castration. These genes are potential diagnostic and therapeutic targets for prostate cancer and benign prostatic hyperplasia. We used microarrays to examine the gene expression profiles in benign prostate adjacent to prostate cancer and prostate cancer in radical prostatectomy specimens and in prostate tissue samples taken 3 days after surgical castration performed for treatment of prostate cancer. Human prostate tissue was obtained from radical prostatectomy samples and from prostate biopsy samples (castrated samples). Benign and malignant tissues samples were microdissected from prostatectomy samples. Tissues were used for RNA isolation and were further processed as samples for microarray. Three prostatectomy samples were used as replicates (benign and malignant prostate). All prostate cancers were Gleason 3+3 pattern. Castrated tissue samples were taken from patients three days after surgical castration for the treatment of advanced or metastasized prostate cancer. Six biopsies were taken from each subject and individual subject samples were used as three replicates in microarray.
2012-06-19 | E-GEOD-32982 | biostudies-arrayexpress
Project description:The prostate gland mainly contains basal and luminal cells constructed as a pseudostratified epithelium. Annotation of prostate epithelial transcriptomes provides a foundation for discoveries that can impact disease understanding and treatment. Here, we describe a whole-genome transcriptome analysis of human benign prostatic basal and luminal populations by using deep RNA sequencing. Combined with comprehensive molecular and biological characterizations, we show that the differential gene expression profiles account for their distinct functional phenotypes. Strikingly, in contrast to luminal cells, basal cells preferentially express gene categories associated with stem cells, neural and neuronal development and RNA processing. Consistent with their expression profiles, basal cells functionally exhibit intrinsic stem-like and proneural properties with enhanced ribosome RNA (rRNA) transcription activity. Of clinical relevance, the treatment failed castration-resistant and anaplastic prostate cancers molecularly resemble a basal-like phenotype. Therefore, we link the cell-type specific gene signatures to subtypes of prostate cancer development, and identify genes associated with patient clinical outcome. Human total RNA profiles of 3 pairs of benign prostatic basal and luminal populations freshly purified from prostate tissues of three prostate cancer patients by deep RNA-seq.
2015-04-30 | E-GEOD-67070 | biostudies-arrayexpress
Project description:Castration-resistant prostate cancer is a lethal disease. The cell type(s) that survive androgen-deprivation remain poorly described despite global efforts to understand the various mechanisms of therapy resistance. We recently identified in wild type mouse prostates a rare population of luminal progenitor cells that we called LSCmed according to their FACS profile (Lin?/Sca-1+/CD49fmed). Here we investigated the prevalence and castration resistance of LSCmed in various mouse models of prostate tumorigenesis. In intact mice, we show that LSCmed prevalence remains low (5-10% of epithelial cells) when prostatic androgen receptor signaling unaltered (malignant Hi-Myc mice) but significantly increases in models exhibiting reduced prostatic androgen receptor signaling, rising up to 30% in premalignant tumors (Pb-PRL mice) and to >80% in castration-resistant prostate tumors driven by Pten loss (Ptenpc-/- mice). LSCmed tolerance to androgen deprivation was demonstrated by their persistence (Ptenpc-/-) or further enrichment (Pb-PRL) 2-3 weeks after castration as evidenced by FACS analysis. Transcriptomic analysis revealed that LSCmed represent a unique cell entity as their gene-expression profile is different from luminal and basal/stem cells, but shares markers of each. Their intrinsic androgen signaling is markedly decreased, which explains why LSCmed tolerate androgen-deprivation. This also enlightens why Ptenpc-/- tumors are castration-resistant since LSCmed represent the most prevalent cell type in this model. We validated CK4 as a specific marker for LSCmed on sorted cells and prostate tissues by immunostaining, allowing for the detection of LSCmed in various mouse prostate specimens. In castrated Ptenpc-/- prostates, BrdU staining revealed massive proliferation of CK4+ cells, further demonstrating their key role in castration-resistant prostate cancer progression. In all, this study identifies LSCmed as a probable source of prostate cancer relapse after androgen deprivation and as a new therapeutic target for the prevention of castrate-resistant prostate cancer.
2017-08-15 | E-MTAB-4991 | biostudies-arrayexpress
Project description:Chromosomal translocations or upregulations involving ETS transcription factor are frequent events in prostate cancer pathogenesis and significantly co-occurrence with p53 or PTEN loss. Caused by the low stabilities of ETS proteins in cytosol, mouse models with aberrant expression of wild type ETS transcription factors had subtle phenotypes and only drive prostate cancer progression in the setting of Pten loss. Here we show that prostate specific aberrant expression of mutated ETV4 (V70P71D72-AAA, ETV4-AAA), which is resistence to COP1 mediated protein degradation, results in more stabilized ETV4 protein in mouse prostate. We found that ETV4-AAA mice develop marked prostatic intraepithelial neoplasia (mPin) and p53-dependent cell senescence within 2 weeks, but without tumor development when aged. Interestingly, ETV4-AAA positive cells reduce dramatically in a PTEN loss background, which means that there is no cooperation between ETV4-AAA and PTEN loss. Aberrant ETV4-AAA expression promotes progression of mPin to prostatic adenocarcinoma in a Tp53 deficiency or haploinsufficiency background. In contrast to PTEN loss induced mouse prostate cancers which loss NKX3.1 expression and resistant to castration therapy, these ETV4-AAA tumor cells well maintain AR and NKX3.1 expression and are sensitive to castration therapy.
2021-01-01 | GSE130311 | GEO
Project description:Androgen signaling is essential for prostate tumorigenesis. The tumor suppressor p53 has been implicated in prostate cancer progression. Recent genome analysis of human prostate cancers demonstrated that both AR gene amplification and TP53 deletion are frequently altered in advanced prostate cancer. However, the biological role of these dual genetic alterations in prostate tumorigenesis is largely unknown. In addition, there are no biologically relevant models that can be used to assess these genetic abnormalities in the prostate. Here, we report a novel mouse model, in which elevated transgenic AR expression and Trp53 deletion occur simultaneously in mouse prostatic epithelium to mimic what happens in human prostate cancer cells. These compound mice developed an earlier onset of high-grade prostatic intraepithelial neoplasia and accelerated prostate tumors. Histological analysis showed pathological lesions resembling prostatic sarcomatoid and basaloid carcinomas with massive squamous differentiation in the above compound mice. RNA-sequencing analyses showed a robust enrichment of the signature genes for human prostatic basal cell carcinomas in the above prostate tumors. The Master Regulator Analysis further identified SOX2 as a transcriptional regulator in prostatic basal cell tumors. Elevated expression of SOX2 and its downstream target genes were detected in prostatic tumors of the compound mice. Chromatin immunoprecipitation analyses implicate a co-regulatory role of AR and SOX2 in the expression of prostatic basal cell signature genes. These results demonstrate a novel mechanism underlying elevated AR expression and Trp53 deletion induced prostate cancer cell trans-differentiation, aggressiveness, and progression.
2019-04-03 | GSE129243 | GEO
Project description:Androgens are a prequisite for the development of human prostate and prostate cancer. Androgen action is mediated via androgen receptor. Androgen ablation therapy is used for the treatment of metastasized prostate cancer. The aim of the study was to identify genes differentially expressed in benign human prostate, prostate cancer and in prostate tissue three days after castration. These genes are potential diagnostic and therapeutic targets for prostate cancer and benign prostatic hyperplasia. We used microarrays to examine the gene expression profiles in benign prostate adjacent to prostate cancer and prostate cancer in radical prostatectomy specimens and in prostate tissue samples taken 3 days after surgical castration performed for treatment of prostate cancer.
2012-06-20 | GSE32982 | GEO