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Genomic Characterization of Metastatic Castration Resistant Prostate Cancer

ABSTRACT: Genomic Characterization of Metastatic Castration Resistant Prostate Cancer

PROVIDER: PRJNA479544 | ENA |

REPOSITORIES: ENA

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Genomic Characterization of Metastatic Castration Resistant Prostate Cancer

Project description:Genomic Characterization of Metastatic Castration Resistant Prostate Cancer

| PRJNA479543 | ENA

Epigenetic Activation and alteration of chromatin structure regulated by NSD2 in metastatic castration-resistant prostate cancer (Hi-C)

Project description:To elucidate the regulation of NSD2 in metastatic castration-resistant prostate cancer(CRPC), we performed Hi-C against castration-sensitive prostate cancer cell line LNCaP and metastatic castration-resistant prostate cancer cell lines, PC3 respectively. In metastatic CRPC, we found specific regions of activation with epigenetic changes.

2024-09-04 | GSE248627 | GEO

Epigenetic Activation and alteration of chromatin structure regulated by NSD2 in metastatic castration-resistant prostate cancer (ChIP-seq)

Project description:To elucidate the regulation of NSD2 in metastatic castration-resistant prostate cancer(CRPC), we performed ChIP-seq of H3K36me2, H3K27me3, H3K4me1, H3K4me3,H3K27ac and NSD2 against castration-sensitive prostate cancer cell line LNCaP and metastatic castration-resistant prostate cancer cell lines, PC3 and DU145, respectively. In metastatic CRPC, we found specific regions of activation with epigenetic changes.

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Epigenetic Activation and alteration of chromatin structure regulated by NSD2 in metastatic castration-resistant prostate cancer (RNA-seq)

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Genomic Characterization of Metastatic Castration Resistant Prostate Cancer

Project description:<p>Biopsies of castration resistant prostate cancer metastases were subjected to whole genome sequencing (WGS), along with RNA-sequencing (RNA-Seq). The overarching goal of the study is to illuminate molecular mechanisms of acquired resistance to therapeutic agents, and particularly androgen signaling inhibitors, in the treatment of metastatic castration resistant prostate cancer (mCRPC).</p>

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Whole Genome Methylation Analysis of Metastatic Castration Resistant Prostate Cancer

Project description:Relatively little is known about how changes in gene copy number (CN) and gene CpG methylation interact to affect specific pathways in metastatic castration-resistant prostate cancer (CRPC). Oligonucleotide array comparative genomic hybridization (aCGH) was performed on DNA isolated from 15 metastatic CRPC samples. Commonly aberrant genes were evaluated in a confirmatory fashion using PCR, aCGH data from primary tumors, and existing CRPC expression data. Array-based comprehensive CpG methylation was assessed on the same sample set. A total of 495 genes (79 gained, 416 deleted) were CN aberrant in ?66% of the samples by aCGH, and 77 (9 amplified, 68 deleted) had statistically concordant expression including gain of AR and loss of PTEN and RB1. Significant CN differences were seen between the genomes of patients with AR-amplified and AR-unamplified tumors, including common loss of AR repressors in AR-unamplified tumors. The majority of CRPC samples were hypermethylated compared to benign prostate tissue. Simultaneous methylation and heterozygous gene deletion occurred in the tumor suppressor RB1 and in HSD17B2, responsible for testosterone metabolism. Establishment of a comprehensive methylation signature and coupling of epigenomic and structural analyses sheds light on the alterations that allow CRPC to circumvent hormonal therapy and may provide new drug targets for what is currently an incurable disease state. 15 tumor samples taken from 14 men with metastatic castration resistant prostate cancer were analyzed, including two samples from the same patient. No control samples were used for this experiment.

2011-12-06 | E-GEOD-34174 | biostudies-arrayexpress

Dysregulated expression of genes in regulatory T cells from metastatic castration-resistant prostate cancer patients

Project description:We analyzed the global gene expression pattern of Tregs between healthy donors and prostate cancer patients. We found that genes related to cell cycle, cellular proliferation, immune responses, hematological system development and function were differentially expressed in Tregs from prostate cancer patients. Total RNA samples of Tregs, isolated from peripheral blood, were obtained from three separate healthy donors and three metastatic castration-resistant prostate cancer patients. Global gene expression pattern was examined by performing GeneChip microarray hybridization. Genes differentially expressed between the two groups of donors were sorted and categorized based on their biological functions.

2013-03-05 | E-GEOD-38043 | biostudies-arrayexpress

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Project description:Prostate cancer is one of the major cancers that seriously affect men's health. It has high morbidity and high mortality, but there is still no ideal molecular markers for the diagnosis and prognosis of prostate cancer. Castration-resistant prostate cancer is associated with wide variations in survival. To determine whether differentially expressed circRNAs in plasma exosomes can be used as a novel biomarker for castration-resistant prostate cancer prognosis, we performed high-throughput circRNA sequencing on 15 pairs of plasma exosomes from 30 metastatic castration-resistant prostate cancer patients, with or without early progression, to screen differentially expressed circRNAs.

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Whole Transcriptomic Sequencing of Metastatic Castration Resistant Prostate Cancer Samples

Project description:We report the gene expression profile of 8 metastatic castration resisistant prostate cancer samples analyzed by paired-end RNA-seq. We found evidence of extensive abnormal splicing as well as several novel fusion genes. Finally, we also observed several recurrent high-confidence somatic mutations. Paired-end RNA-seq by rRNA depletion

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Effects of PSF knockdown in castration-resistant prostate cancer cells

Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. Androgen-deprivation therapy is the first-line treatment strategy for advanced prostate cancer. However, many tumors develop to castration-resistant prostate cancer (CRPC) and relapse. Thus, analyzing key factors for development of CRPC is important. We found PSF functions as RNA binding protein and transcription factor to promote castration-resistant tumor growth. High expression of PSF in metastatic prostate cancer tissue indicates the clinical relevance. In order to investigate the PSF function in CRPC cells, we performed gene expression in CRPC model cells derived from AR-positive prostate cancer cell lines after siPSF treatment.

2017-12-24 | GSE100239 | GEO

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