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Clinical testing of transcriptome-wide expression classifiers in high-risk localized and metastatic prostate cancer starting androgen deprivation therapy in the STAMPEDE abiraterone and docetaxel Phase 3 trials

ABSTRACT: Gene expression study of the STAMPEDE abiraterone and docetaxel randomized controlled trials

ORGANISM(S): Homo sapiens

PROVIDER: GSE224644 | GEO | 2025/08/27

REPOSITORIES: GEO

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Abiraterone acetate and di-n-butyl phthalate (DBP) response in a human fetal testis xenograft bioassay

Project description:The goal of this study was to determine the effects of a well-characterized anti-androgen, abiraterone acetate, and a suspected human anti-androgen, di-n-butyl phthalate (DBP) on the androgenic function of human fetal testis. Human fetal testis was xenografted into the renal subcapsular space of castrated male athymic nude mice. Hosts were treated with hCG to stimulate testosterone production in the xenografts, and were concurrently treated with either abiraterone acetate or DBP. While abiraterone acetate (14 d, 75 mg/kg/d p.o.) dramatically reduced testosterone and the weights of androgen-sensitive host organs, DBP (14 d, 500 mg/kg/d p.o.) had no effect on androgenic endpoints. Three paired analyses were performed using the LIMMA package in R (commands lmfit and eBayes), with the Benjamini-Hochberg correction for multiple comparisons (Smyth 2005): vehicle-treated xenografts vs. unimplanted testis (n=5), abiraterone-treated xenografts vs. matched control xenografts (n=3), and DBP-treated xenografts vs. matched control xenografts (n=3). There were significant differences in gene expression between grafted and ungrafted samples, including dramatic upregulation of microRNAs. Gene expression analysis also showed that abiraterone decreased expression of genes related to cell differentiation, while DBP induced expression of oxidative stress response genes and decreased expression of factors related to embryonic development. 17 xenograft samples were analyzed, including 5 unimplanted samples, 6 vehicle treated xenografts, 3 abiraterone acetate-treated xenografts, and 3 DBP-treated xenografts. Samples were paired (derived from the same donor tissue) for each comparison: vehicle vs. unimplanted (n=5), abiraterone vs. vehicle (n=3), and DBP vs. vehicle (n=3).

2013-10-31 | E-GEOD-49244 | biostudies-arrayexpress

Abiraterone resistance in prostate cancer cells

Project description:Abiraterone resistance in prostate cancer cells

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Expression data from prostate cancer cell lines C4-2B (docetaxel sensitive) and TaxR (docetaxel resistant) cells

Project description:Prostate cancer C4-2B cells were cultured in docetaxel in a dose-escalation manner. After nine months selection, cells were able to divide freely in 5 nM docetaxel, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for docetaxel resistance in TaxR cells. Docetaxel resistant TaxR cells were selected from C4-2B cells during long time docetaxel treatment. Genes responsible for docetaxel resistance were identified using C4-2B vs. TaxR RNA extraction and hybridization on Affymetrix microarrays.

2013-08-01 | E-GEOD-47040 | biostudies-arrayexpress

Expression data from prostate cancer cell lines C4-2B (docetaxel sensitive) and TaxR (docetaxel resistant) cells

2013-08-01 | GSE47040 | GEO

Androgen deprivation therapy plus abiraterone or docetaxel as neoadjuvant therapy for very-high-risk prostate cancer: a pooled analysis of two phase II trials.

Project description:Objective: The study aimed to compare the efficacy and safety of androgen deprivation therapy (ADT) with abiraterone or docetaxel versus ADT alone as neoadjuvant therapy in patients with very-high-risk localized prostate cancer. Methods: This was a pooled analysis of two single-center, randomized, controlled, phase II clinical trials (ClinicalTrials.gov: NCT04356430 and NCT04869371) conducted from December 2018 to March 2021. Eligible participants were randomly assigned to the intervention (ADT plus abiraterone or docetaxel) and control (ADT alone) groups at a 2:1 ratio. Efficacy was evaluated by pathological complete response (pCR), minimal residual disease (MRD), and 3-year biochemical progression-free survival (bPFS). Safety was also analyzed. Results: The study included 42 participants in the ADT group, 47 in the ADT plus docetaxel group, and 48 in the ADT plus abiraterone group. A total of 132 (96.4%) participants had very-high-risk prostate cancer, and 108 (78.8%) had locally advanced disease. The ADT plus docetaxel group (28%) and ADT plus abiraterone group (31%) had higher rates of pCR or MRD (p = 0.001 and p < 0.001) compared with the ADT group (2%). The 3-year bPFS was 41.9% (95% CI: 26.6-57.2), 51.1% (95% CI: 36.8-65.4), and 61.2% (95% CI: 45.5-76.9), respectively. Significant difference was found among groups in terms of bPFS (p = 0.037). Conclusion: Compared with ADT alone, neoadjuvant therapy with ADT plus docetaxel or abiraterone could achieve better pathological outcomes (pCR or MRD) for very-high-risk localized prostate cancer. The ADT plus abiraterone group showed longer bPFS than ADT alone. The combination regimens were tolerable.

| S-EPMC10331422 | biostudies-literature

PLK1 Inhibitors and Abiraterone Synergistically Disrupt Mitosis and Kill Cancer Cells of Disparate Origin Independently of Androgen Receptor Signaling

Project description:We found that synergy between the antiandrogen abiraterone and Plk1 inhibitors was completely independent of abiraterone's effects on AR signaling. To identify AR-independent effects of abiraterone we designed a comprehensive RNA seq experiment. This identified an AR-independent synergy-specific gene set signature that was induced by abiraterone treatment and was dominated by gene sets related to mitosis and the mitotic spindle. AR-independent effects of abiraterone were isolated by including an enzalutamide treatment arm and by utilizing cancer cell lines that do not express the AR. Synergy-specific gene expression changes were identified by using cell lines that responded synergistically or non-synergistically to combined abiraterone and onvansertib.

2023-01-24 | GSE217537 | GEO

Abiraterone resistance in prostate cancer cells

Project description:Castration resistant prostate cancer (CRPC) develops resistance to antiandrogens affecting Androgen Receptor (AR) signaling through a variety of mechanism. Because of this, the efficacy of androgen receptor targeted therapy remains limited for many patients with CRPC. We developed C42B-Abiraterone (Abi) and resistance cells to study changes in transcriptomic profile compared to parental cells.

2023-01-01 | GSE220467 | GEO

RNA sequencing analysis of VCaP cells resistant to abiraterone

Project description:Here, we analyze gene expression of prostate cancer cell line VCaP (VCaP WT) and VCaP after long time treatment with abiraterone (VCaP AA) in order to investigate possible resistance mechanisms to second-generation antiandrogens.

2024-06-30 | GSE196523 | GEO

Identificatinon of differentially expressed genes in Docetaxel-resistant cell lines PC3 and DU145 after combination treatment with RU486 and docetaxel

Project description:Upregulation of the glucocorticoid receptor (GR) has been identified as a possible bypass mechanism in CRPC. Recently, it has been demonstrated that the combination of docetaxel with mifepristone (D+M), an inhibitor of the GR, reinduces sensitivity to docetaxel in docetaxel resistant cell models. This study was designed to uncover and characterize molecular mechanisms responsible for this observation.

2023-12-31 | GSE233647 | GEO

Expression data from prostate cancer Docetaxel-resistant cells

Project description:Docetaxel is the standard first line therapy for hormone-refractory prostate cancer patients. Here we generated models of Docetaxel resistance in prostate cancer cells to study the molecular pathways that drive the acquisition of resistance to this therapy. We used microarrays to detail the global program of gene expression underlying the acquisition of Docetaxel resistance in prostate cancer cells.

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