Human gut metagenome
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR212845_1.fastq.gz | Fastqsanger.gz | |||
| DRR212845_2.fastq.gz | Fastqsanger.gz | |||
| DRR212846_1.fastq.gz | Fastqsanger.gz | |||
| DRR212846_2.fastq.gz | Fastqsanger.gz | |||
| DRR212847_1.fastq.gz | Fastqsanger.gz |
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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: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:In analyzing transcriptomic data from a clinical trial of neoadjuvant-intensive Androgen Deprivation Therapy, we observed increased mRNA expression of the hallmark antiapoptotic gene BCL2 in the prostate tumors of treated patients versus those of untreated patients. We showed that BCL2 overexpressed LNCaP cells exhibited resistance to prolonged androgen deprivation therapy, indicating that BCL2-overexpression leads to castration resistance and cellular plasticity.Our study indicating that BCL2 overexpression may act as a major driver of early castration resistance in prostate cancer cells.
2025-05-15 | GSE273736 | 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: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:The ligand-activated androgen receptor is a transcription factor that drives prostate cancer growth. Blocking androgen-activation of androgen receptor via androgen deprivation therapy is the default treatment for metastatic prostate cancer. Despite initial remissions, androgen deprivation invariably fails and prostate cancer progresses to castration-recurrent disease, which still relies on aberrantly activated androgen receptor. Alternative approaches are needed to inhibit androgen receptor action in prostate cancer that has failed androgen deprivation therapy. Our laboratory has been exploring the therapeutic potential of a non-canonical androgen receptor signaling mechanism wherein androgen receptor stimulates another transcription factor, Serum Response Factor. Serum Response Factor-mediated androgen receptor action correlates with prostate cancer progression and is enriched in castration-recurrent prostate cancer. Inhibiting Serum Response Factor-dependent androgen receptor action may be an effective treatment strategy following failure of androgen deprivation therapy but remains poorly understood. We have recently isolated UPF1 and RCOR1 as putative novel mediators of Serum Response Factor-dependent androgen receptor action. Here, we perform RNA-Seq assays to determine the contribution of UPF1 and RCOR1 to the androgen response of prostate cancer cells.
2025-05-15 | GSE248034 | GEO
Project description:Radiotherapy (RT) with or without androgen deprivation therapy (ADT) is standard salvage therapy for men with local or biochemical recurrence of prostate cancer after prostatectomy, but there is an unmet need for biomarkers to identify potential non-responders. We hypothesized that androgen receptor splice variants (ARVs) are detectable in primary prostate cancer and may modulate response to salvage RT+ADT. We identified a retrospective cohort of prostate cancer patients treated with prostatectomy followed by salvage RT + ADT, and we performed targeted RNA-seq of archival formalin-fixed paraffin-embedded prostatectomy samples to comprehensively characterize the landscape of ARVs.
2026-01-07 | GSE268636 | GEO
Project description:Androgen deprivation therapy (ADT) is a foundational treatment for advanced prostate cancer, but more than half of patients treated with ADT experience debilitating cognitive impairments in domains known to be mediated by the hippocampus and prefrontal cortex. Unfortunately, there are few treatments to prevent or reverse these changes from occuring, thus severely decreasing quality of life in patients. To begin studying these deficits, surgically castrated rats were used to model cognitive impairments associated with the spatial learning and executive function, then chronically treated with the multimodal antidepressant, vortioxetine, as in intervention to reverse these impairments. Vortioxetine effectively rescued cognitive deficits in after surgical castration, and increased resposivity in in vivo evoked local field potentials within the Schaeffer Collateral-CA1 pathway and the ventral hippocampus-mPFC pathway. Surgical castration also induced significant changes in gene expression within the mPFC and the dorsal hippcampus, whereas vortioxetine had little effect. Pathway analysis revealed that androgen depletion altered pathways related to synaptic plasticity. These results suggest that these two regions may be vulnerable to ADT, contributing to cognitive impairment in prostate cancer patients. Further, vortioxetine may be a candidate to improve cognition in patients that experience cognitive decline after androgen deprivation therapy for prostate cancer and may do so by restoring molecular and circuit level plasticity-related mechanisms compromised by ADT.
2023-10-04 | GSE236207 | 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