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Temporal evolution of cellular heterogeneity during the progression to advanced, AR-negative prostate cancer [RRBS]

ABSTRACT: Temporal evolution of cellular heterogeneity during the progression to advanced, AR-negative prostate cancer [RRBS]

PROVIDER: PRJNA636399 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11903134.fastq.gz	Fastqsanger.gz
	SRR11903135.fastq.gz	Fastqsanger.gz
	SRR11903136.fastq.gz	Fastqsanger.gz
	SRR11903137.fastq.gz	Fastqsanger.gz
	SRR11903138.fastq.gz	Fastqsanger.gz

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Temporal evolution of cellular heterogeneity during the progression to advanced, AR-negative prostate cancer [RRBS]

Project description:Despite advances in the development of highly effective androgen receptor (AR)-directed therapies for the treatment of men with advanced prostate cancer, acquired resistance ultimately ensues. A significant subset of patients with resistant disease develop AR-null, androgen-indifferent tumors that lose their luminal identify and display neuroendocrine features (neuroendocrine prostate cancer (NEPC)). Utilizing a genetically engineered mouse model, we have characterized the synergy between N-Myc overexpression and RB1 loss-of-function which results in the formation of AR-negative, poorly differentiated tumors with high metastatic potential. Single-cell-based approaches revealed striking changes to the transcriptome and chromatin accessibility during the transition to NEPC. Global DNA methylation and the N-Myc cistrome are redirected following RB1 loss. Altogether, our data provide new insight into the progression to NEPC.

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Project description:Despite advances in the development of highly effective androgen receptor (AR)-directed therapies for the treatment of men with advanced prostate cancer, acquired resistance to such therapies frequently ensues. A significant subset of patients with resistant disease develop AR-negative tumors that lose their luminal identity and display neuroendocrine features (neuroendocrine prostate cancer (NEPC)). The cellular heterogeneity and the molecular evolution during the progression from AR-positive adenocarcinoma to AR-negative NEPC has yet to be characterized. Utilizing a new genetically engineered mouse model, we have characterized the synergy between Rb1 loss and MYCN (encodes N-Myc) overexpression which results in the formation of AR-negative, poorly differentiated tumors with high metastatic potential. Single-cell-based approaches revealed striking temporal changes to the transcriptome and chromatin accessibility which have identified the emergence of distinct cell populations, marked by differential expression of Ascl1 and Pou2f3, during the transition to NEPC. Moreover, global DNA methylation and the N-Myc cistrome are redirected following Rb1 loss. Altogether, our data provide insight into the progression of prostate adenocarcinoma to NEPC.

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