E-GEOD-48403
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA209978
PROVIDER: E-GEOD-48403 | ExpressionAtlas | 2019-05-14
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Androgen deprivation is a standard of care front-line therapy for human prostate cancer, however, majority of patients will eventally develop resistance to androgen deprivation. In this study, using a human prostate cancer xenograft model -LuCaP35, we examiend the gene expression changes after castration. We compare the gene expression of 5 LuCaP35 xenografts from non-treated mice (Control), and 5 androgen-deprived LuCaP35 xenografts from castrated mice (Castration).
2011-12-06 | E-GEOD-33316 | biostudies-arrayexpress
Project description:Prostate cancer is the most common cancer in men and androgen receptor (AR) downstream signalings promote prostate cancer progression. Although androgen deprivation therapy is effective for treating prostate cancer, most tumors relapsed as castration-resistant prostate cancer (CRPC). We performed ChIP-seq analysis to investigate the role of important transcription factors and histone modifications using AR positive prostate cancer cells, LNCaP, CRPC model cells, 22Rv1 and DU145 cells.
2021-05-01 | GSE146886 | GEO
Project description:Androgen deprivation is a standard of care front-line therapy for human prostate cancer, however, majority of patients will eventally develop resistance to androgen deprivation. In this study, using a human prostate cancer xenograft model -LuCaP35, we examiend the gene expression changes after castration.
2011-12-06 | GSE33316 | GEO
Project description:Following androgen ablation therapy (AAT), the vast majority of prostate cancer patients develop treatment resistance with a median time of 18-24 months to disease progression. To identify molecular targets that aid in prostate cancer cell survival and contribute to the androgen independent phenotype, we evaluated changes in LNCaP cell gene expression during 12 months of androgen deprivation. At time points reflecting critical growth and phenotypic changes, we performed Affymetrix expression array analysis to examine the effects of androgen deprivation during the acute response, during the period of apparent quiescence, and during the emergence of highly proliferative, androgen-independent prostate cancer cells (LNCaP-AI). We discovered alterations in gene expression for a host of molecules associated with promoting prostate cancer cell growth and survival, regulating cell cycle progression, apoptosis and adrenal androgen metabolism, in addition to AR co-regulators and markers of neuroendocrine disease. These findings illustrate the complexity and unpredictable nature of cancer cell biology and contribute greatly to our understanding of how prostate cancer cells likely survive AAT. The value of this longitudinal approach lies in the ability to examine gene expression changes throughout the cellular response to androgen deprivation; it provides a more dynamic illustration of those genes which contribute to disease progression in addition to specific genes which constitute a malignant androgen-independent phenotype. In conclusion, it is of great importance that we employ new approaches, such as the one proposed here, to continue exploring the cellular mechanisms of therapy resistance and identify promising targets to improve cancer therapeutics. Experiment Overall Design: To identify molecular targets that aid in prostate cancer cell survival and contribute to the androgen independent phenotype, we evaluated changes in LNCaP cell gene expression during 12 months of androgen deprivation. At time points reflecting critical growth and phenotypic changes, we performed Affymetrix expression array analysis to examine the effects of androgen deprivation during the acute response, during the period of apparent quiescence, and during the emergence of highly proliferative, androgen-independent prostate cancer cells (LNCaP-AI).
2008-04-07 | E-GEOD-8702 | biostudies-arrayexpress
Project description:Androgen receptor (AR) signaling is a major driver and therapy target in prostate cancer. Several inhibitors of AR function are approved for different stages of the disease and their impact on downstream gene transcription has been described. However, the ensuing effects of androgen and anti-androgens at the protein level are less well understood. Here, we focused on the AR inhibitor darolutamide which has recently been approved for non-metastatic castration-resistant prostate cancer. Here we determined the impact of darolutamide, a recently approved AR antagonist which significantly extends progression-free and overall survival in non-metastatic CRPC (31, 32), on the prostate cancer proteome. We first determined the direct binding between darolutamide and the AR in living prostate cancer cells in a label-free context using the cellular high throughput thermal shift assay (CETSA HT). We then generated comprehensive proteomic profiles of prostate cancer cells treated with androgen and darolutamide, and compared them with transcriptomic profiles. We found a generally high concordance between proteomic and transcriptomic data, both on the level of detected expressed genes and their protein products, as well as in terms of the corresponding biological programs. However there were cases where protein and gene expression levels were not regulated in parallel, suggesting an additional post-transcriptional regulation step controlling protein abundance to occur in several instances.
2023-02-17 | PXD036962 | Pride
Project description:Microbiome analysis of prostate cancer patients treated with androgen deprivation therapy.
| PRJDB9379 | ENA
Project description:Benign prostate tissue and prostate cancer tissue (untreated, androgen deprivation therapy responding, or castrate-resistant) was collected from patients at the time of transurethral resection of the prostate surgery. 24 samples, technical replicates.
2012-12-01 | E-GEOD-28680 | biostudies-arrayexpress
Project description:Benign prostate tissue and prostate cancer tissue (untreated, androgen deprivation therapy responding, or castrate-resistant) was collected from patients at the time of transurethral resection of the prostate surgery.
2012-12-01 | GSE28680 | GEO
Project description:Prostate cancer is a leading cause of cancer-related death and morbidity worldwide. Androgen deprivation therapy (ADT) is the cornerstone of management for advanced disease. The use of androgen deprivation therapies is associated with multiple side effects, including metabolic syndrome and truncal obesity. At the same time, obesity has been associated with both prostate cancer development and disease progression, linked to its effects on chronic inflammation at a tissue level. The connection between androgen deprivation therapy, obesity, inflammation, and prostate cancer progression is well-established in clinical settings; however, an understanding of the changes in adipose tissue at the molecular level induced by castrating therapies is missing. Here we investigated the transcriptional changes in periprostatic fat tissue induced by profound androgen deprivation therapy in a group of patients with high-risk tumours compared to a matching untreated cohort. We find that androgen deprivation therapy is associated with a pro-inflammatory and obesity-like adipose tissue microenvironment. This study suggests that the beneficial effect of androgen deprivation therapy may be partially counteracted by metabolic and inflammatory side effects in the adipose tissue surrounding the prostate.
| EGAS00001003286 | EGA
Project description:Purpose: The goals of this study is to compare NGS-derived Androgen Deprivation Therapy (ADT) resistant miRNome profiling to Androgen Deprivation Therapy (ADT) sensitive miRNome profile in African American prostate cancer cells and validate by reverse transcription polymerase chain reaction (qRT–PCR) methods. Method: Mirco-RNA were isolated from different CaP cells who were sensitive and resistant to Androgen Deprivation Therapy (ADT). Total micro-RNA were subjected to miRNA-Seq. Results: We performed whole miRNA-Seq analysis through paired-end deep sequencing to systematically investigate the molecular features of different CaP cell models- RC-77-N, RC-77T/E, RCC7T/E-ADT, RCC7T/E-CD133-plus, E006AA-hT and E006AA-hT-ADT. Conclusions: Our study represents the first detailed analysis of African American ADT resistant miRNome, with biologic replicates, generated by miRNA-seq technology.
2019-07-09 | GSE116636 | GEO