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Histological heterogeneity in primary prostate

ABSTRACT: Histological heterogeneity in primary prostate

PROVIDER: PRJNA1028110 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26385010_1.fastq.gz	Fastqsanger.gz
	SRR26385010_2.fastq.gz	Fastqsanger.gz
	SRR26385011_1.fastq.gz	Fastqsanger.gz
	SRR26385011_2.fastq.gz	Fastqsanger.gz
	SRR26385016.fastq.gz	Fastqsanger.gz

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Spatial transcriptomics reveals unexpected histological heterogeneity in primary prostate

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Extensive androgen receptor enhancer heterogeneity in primary prostate cancer patients underlies transcriptional diversity and metastatic potential

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Histological heterogeneity in primary prostate

Project description:This SuperSeries is composed of the SubSeries listed below.

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Primary prostate organoid transcriptomic profile in co-culture with primary prostate stroma

Project description:Organotypic in vitro culture is useful to model mammalian disease in numerous tissues. Normal epithelial differentiation and carcinogenesis both undergo in vivo regulation by stroma, but current culture methods exclude stroma. To mimic this in vivo environment, we developed and characterized a human 3D prostate organoid co-culture model that incorporates prostate stroma. Primary prostate stromal cells supported increased organoid formation and expressed growth factors and WNT-related genes involved in epithelial differentiation. Organoid branching occurred distal to physical contact with stromal cells, demonstrating non-random branching. Tumoroids derived from primary prostate cancer maintained differential expression of the prostate cancer marker AMACR only in the presence of stroma. Stroma-induced phenotypes were similar in all patients examined, yet maintained inter-patient heterogeneity in the degree of response. Addition of stroma to in vitro organoid culture recapitulated the in vivo microenvironment by inducing organization of benign organoids into branching structures and preserving prostate cancer phenotypes.

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Primary prostate organoid transcriptomic profile in co-culture with primary prostate stroma

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DNA methylation profiling across six histological states of prostate cancer

Project description:In spite of its prevalence as one of the world’s leading malignancies, prostate cancer (PCa) continues to evade molecular taxonomic sub-classification. However, gross clinical differences are observed within the umbrella term ‘prostate adenocarcinoma’; the majority of tumors appear indolent in nature, whilst a subset manifest aggressively. Contributing factors towards this resistance to molecular classification are an atypically low mutation frequency and a poorly delineated pathobiology. Conversely, epigenetic changes are evidenced to be amongst the earliest and most-widespread aberrations in PCa . We thus hypothesized that delineating epigenomic alterations during the stepwise progression of PCa would improve our understanding of the disease pathobiology and the molecular underpinning of indolent and aggressive tumors. Herein, we report the first epigenomic roadmap of prostate tumorigenesis, in which we dissected DNA methylation and microRNA expression in enriched epithelial cells across the entire trajectory of PCa, through tumor initiation, primary disease and metastatic dissemination. Infinium Human Methylation450K Beachip (Illumina) technology was employed to assess the methylation status of >485,000 CpG sites throughout the genome across six histological stages of prostate cancer (PCa) tumorigenesis: benign (n=10), proliferative inflammatory atrophy (PIA; n=7), high grade prostatic intra-epithelial neoplasia (HGPIN; n=6), indolent PCa (PCI, n=7), agressive PCa (PCA; n=8) and lethal metastatic PCa (PCM; n=6). Three peripheral blood lymphocytes (PBL) samples were also included for control purposes.

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