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CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [ChIP-seq]

ABSTRACT: CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [ChIP-seq]

PROVIDER: PRJNA744543 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15065546.fastq.gz	Fastqsanger.gz
	SRR15065547.fastq.gz	Fastqsanger.gz
	SRR15065548.fastq.gz	Fastqsanger.gz
	SRR15065549.fastq.gz	Fastqsanger.gz
	SRR15065550.fastq.gz	Fastqsanger.gz

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CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer

Project description:CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer

| PRJNA744541 | ENA

CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [RNA-Seq]

Project description:CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [RNA-Seq]

| PRJNA744547 | ENA

CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [RNA-Seq]

Project description:High-dose testosterone (high-T) treatment can effectively suppress the growth of castration-resistant prostate cancer (CRPC) in preclinical studies using patient-derived xenograft (PDX) models and in clinical trials of CRPC. However, the molecular basis for this treatment remains to be determined. In previous studies, we have shown that androgen receptor (AR) can function as a transcription repressor to suppress the expression of genes mediating DNA replication via recruitment of hypophosphorylated retinoblastoma protein (Rb). However, it is unclear how Rb globally mediates this transcriptional repressor activity of AR and contributes to the tumor-suppressive effect of high-dose androgen in CRPC.

2022-02-14 | GSE179687 | GEO

CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [ChIP-seq]

2022-02-14 | GSE179684 | GEO

CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-02-14 | GSE179688 | GEO

Different doses of androgens induce the expression of distinct gene expression programs [ChIP-Seq]

Project description:Most prostate cancers express the androgen receptor (AR), and tumor growth and progression are facilitated by exceptionally low levels of systemic or intratumorally produced androgens. Paradoxically, high dose androgens have also shown considerable efficacy in the treatment of patients with late-stage metastatic PCa. In probing the mechanisms that enable cells to recognize and respond to different levels of the same hormone, it was determined that low levels of androgens, functioning through an AR monomer, facilitates a non-genomic activation of the mTOR signaling pathway to drive proliferation. Conversely, high dose androgens facilitate the formation of AR dimers to suppress c-MYC expression, inhibit proliferation and drive a transcriptional program associated with a differentiated phenotype. These findings highlight the inherent liabilities in current approaches used to inhibit AR action in PCa and are instructive as to strategies that can be used to develop new therapeutics for this disease and other androgenopathies.

2024-07-09 | GSE262744 | GEO

Different doses of androgens induce the expression of distinct gene expression programs (ATAC-Seq)

2024-07-09 | GSE247591 | GEO

Different doses of androgens induce the expression of distinct gene expression programs (RNA-Seq)

2024-07-09 | GSE247592 | GEO

Intraprostatic Androgens and Androgen-Regulated Gene Expression Persist Following Testosterone Suppression

Project description:Introduction: Androgen deprivation therapy (ADT) remains the primary treatment for advanced prostate cancer (PCa). The efficacy of ADT has not been rigorously evaluated by demonstrating suppression of prostatic androgen activity at the target tissue and molecular level. We determined the efficacy and consistency of medical castration in suppressing prostatic androgen levels and androgen-regulated gene-expression. Design: Androgen levels and androgen-regulated gene-expression (by microarray-profiling, qRT-PCR and immunohistochemistry) were measured in prostate samples from a clinical trial of short-term castration (1 month) using the GnRH-antagonist, Acyline, vs. placebo in healthy men. To assess the effects of long-term ADT, gene-expression measurements were evaluated at baseline and after 3, 6 and 9 months of neoadjuvant ADT in prostatectomy samples from men with localized PCa. Results: Medical castration reduced tissue androgens by 75% and reduced the expression of several androgen-regulated genes (NDRG1, FKBP5, TMPRSS2). However, many androgen-responsive genes, including the androgen receptor (AR) and PSA, were not suppressed after short-term castration, nor after 9 months of neoadjuvant ADT. Significant heterogeneity in PSA and AR protein expression was observed in PCa samples at each time-point of ADT. Conclusions: Medical castration based on serum testosterone levels cannot be equated with androgen ablation in the prostate microenvironment. Standard androgen deprivation does not consistently suppress androgen-dependent gene-expression. Suboptimal suppression of tumoral androgen activity may lead to adaptive cellular changes allowing PCa cell survival in a low androgen environment. Optimal clinical efficacy will require testing of novel approaches targeting complete suppression of systemic and intracrine contributions to the prostatic androgen microenvironment. Keywords: prostate, androgen, Acyline, microarray, immunohistochemistry

2007-10-25 | GSE8466 | GEO

Impact of CDK4-deficiency on EM-BM-5-myc driven B-lymphoma

Project description:Impact of CDK4-deficiency on EM-BM-5-myc driven B-lymphoma By crossing mating CDK4 Knockout mice with EM-BM-5-myc mice,We found CDK4-deficiency enhances the EM-BM-5-myc induced B-lymphoma.We further to discover the molecular mechanism B-lymphoma cells form the cdk4+/+ EM-BM-5-myc and cdk4-/-EM-BM-5-myc mice and then culturing for RNA extraction and hybridization on Affymetrix microarrays.

2012-12-16 | E-GEOD-21683 | biostudies-arrayexpress

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