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Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC [RNA-seq]

ABSTRACT: Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC [RNA-seq]

PROVIDER: PRJNA880856 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21590551_1.fastq.gz	Fastqsanger.gz
	SRR21590551_2.fastq.gz	Fastqsanger.gz
	SRR21590552_1.fastq.gz	Fastqsanger.gz
	SRR21590552_2.fastq.gz	Fastqsanger.gz
	SRR21590553_1.fastq.gz	Fastqsanger.gz

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Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC

Project description:Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC

| PRJNA880855 | ENA

Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC [ATAC-seq]

Project description:Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC [ATAC-seq]

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Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC [RNA-seq: patient biopsies]

Project description:Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC [RNA-seq: patient biopsies]

| PRJNA954869 | ENA

Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC [RNA-seq]

Project description:Testosterone is the canonical growth factor of prostate cancer but can paradoxically suppress its growth when present at supraphysiological levels. We have previously demonstrated that the cyclical administration of supraphysiological androgen (SPA), entitled Bipolar Androgen Therapy (BAT), can result in tumor regression and clinical benefit for patients with castration-resistant prostate cancer. However, predictors and mechanisms of response and resistance have been ill-defined. Here we show that growth inhibition of prostate cancer models by SPA requires high androgen receptor (AR) activity and is driven in part by downregulation of MYC. Using matched sequential patient biopsies, we show that high pre-treatment AR activity predicts downregulation of MYC, clinical response, and prolonged progression-free and overall survival for patients on BAT. BAT induced strong downregulation of AR in all patients, which is shown to be a primary mechanism of acquired resistance to SPA. Acquired resistance can be overcome by alternating SPA with the AR inhibitor enzalutamide, which induces adaptive upregulation of AR and re-sensitizes prostate cancer to SPA. This work identifies high AR activity score as a predictive biomarker of response to BAT and supports a new treatment paradigm for prostate cancer involving alternating between AR inhibition and activation

2022-11-01 | GSE213443 | GEO

Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC [ATAC-seq]

2022-11-01 | GSE213437 | GEO

Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC [RNA-seq: patient biopsies]

2023-04-12 | GSE229555 | GEO

Androgen receptor activity in prostate cancer dictates efficacy of bipolar androgen therapy through MYC.

Project description:Testosterone is the canonical growth factor of prostate cancer but can paradoxically suppress its growth when present at supraphysiological levels. We have previously demonstrated that the cyclical administration of supraphysiological androgen (SPA), termed bipolar androgen therapy (BAT), can result in tumor regression and clinical benefit for patients with castration-resistant prostate cancer. However, predictors and mechanisms of response and resistance have been ill defined. Here, we show that growth inhibition of prostate cancer models by SPA required high androgen receptor (AR) activity and were driven in part by downregulation of MYC. Using matched sequential patient biopsies, we show that high pretreatment AR activity predicted downregulation of MYC, improved clinical response, and prolonged progression-free and overall survival for patients on BAT. BAT induced strong downregulation of AR in all patients, which is shown to be a primary mechanism of acquired resistance to SPA. Acquired resistance was overcome by alternating SPA with the AR inhibitor enzalutamide, which induced adaptive upregulation of AR and resensitized prostate cancer to SPA. This work identifies high AR activity as a predictive biomarker of response to BAT and supports a treatment paradigm for prostate cancer involving alternating between AR inhibition and activation.

| S-EPMC9711876 | biostudies-literature

Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC

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

2022-11-01 | GSE213444 | GEO

Amplitude modulation of androgen signaling by c-MYC [RNA-Seq]

Project description:Androgen-stimulated growth of the molecular apocrine breast cancer is mediated by an androgen receptor (AR)-regulated transcriptional program. Through profiling the genomic licalizations of AR and its co-regulators FOXA1 and TCF7L2 in MDA-MB-453 breast cancer cells, we revealed the molecular details of the AR-centered regulatory network. We further identified that c-MYC is a key downstream target co-regulated by AR, FOXA1 and TCF7L2, and reinforces the transctiopnal activation of androgen-responsive genes in this subtype of breast cancers. MDA-MB-453 breast cancer cells were transfected with control of MYC siRNA for 48 h, followed by treatment with 10nM DHT or vehicle for 6 h. The cells were subjected to mRNA purification and library praparation for RNA-seq on Illumina HiSeq2000 platform.

2013-03-16 | E-GEOD-45202 | biostudies-arrayexpress

Amplitude modulation of androgen signaling by c-MYC [ChIP-Seq]

Project description:Androgen-stimulated growth of the molecular apocrine breast cancer is mediated by an androgen receptor (AR)-regulated transcriptional program. Through profiling the genomic licalizations of AR and its co-regulators FOXA1 and TCF7L2 in MDA-MB-453 breast cancer cells, we revealed the molecular details of the AR-centered regulatory network. We further identified that c-MYC is a key downstream target co-regulated by AR, FOXA1 and TCF7L2, and reinforces the transctiopnal activation of androgen-responsive genes in this subtype of breast cancers. AR and FOXA1 ChIP-seq were performed in MDA-MB-453 breast cancer cells with treatment of 5a-dihydrotestosterone (DHT) for 16 h. TCF7L2 ChIP-seq was performed in MDA-MB-453 cells treated with vehicle or DHT for 16 h, respectively. MYC ChIP-seq was performed in MDA-MB-453 cells following 6 h DHT stimulation.

2013-03-16 | E-GEOD-45201 | biostudies-arrayexpress

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