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Genomic Characterization of Metastatic Castration Resistant Prostate Cancer

ABSTRACT: Genomic Characterization of Metastatic Castration Resistant Prostate Cancer

PROVIDER: PRJNA479543 | 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

| PRJNA479544 | 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

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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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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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.

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Inhibition of HIF1 signaling as a therapeutic option for metastatic castration-resistant prostate cancer.

Project description:Metastatic prostate cancer is a deadly disease, due to the lack of efficient therapies. PTEN and TP53 are the most frequently mutated tumor suppressor genes in metastatic PCa, but the molecular and cellular events underlying tumor aggressivity and treatment resistance are incompletely understood. We have previously shown that Pten/Trp53(i)-/- mice, in which both Pten and Trp53 are selectively inactivated in prostatic luminal cells at adulthood, develop aggressive intraductal prostate carcinoma (IDC) and liver metastases. By combining single cell and spatial transcriptomic, as well as flow cytometry analyses, we now demonstrate that prostatic tumors of such mice are hypoxic and are within a complex immune infiltrate, including neutrophils, as well as TREM2+ macrophages and CCR2+ myeloid cells. Moreover, we uncovered that genetic inactivation of Hif1a in PECs of Pten/Trp53(i)pe-/- mice or pharmacological inhibition of HIF1 signaling does not impair IDC formation and epithelial cell plasticity induced by Trp53 deficiency, but promotes neutrophil chemotaxis. In addition, systemic HIF1 inhibition reduces CCR2+ myeloid cell infiltration, and antagonizing these cells or neutrophils overcomes castration resistance in primary tumors and reduces the size of liver metastatic niches. Importantly, we demonstrate that pharmacological HIF1 inhibition also overcomes castration resistance of PTEN/p53-deficient prostatic tumors, and eradicates liver metastatic niches with an increased efficiency compared to the myeloid cells antagonists. Thus, pharmacological inhibition of HIF1 signaling is a promising therapeutic approach for metastatic castration-resistant prostate cancer.

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