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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage (Whole Exome-seq)

ABSTRACT: Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage (Whole Exome-seq)

PROVIDER: PRJNA484870 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7651692_1.fastq.gz	Fastqsanger.gz
	SRR7651692_2.fastq.gz	Fastqsanger.gz
	SRR7651693_1.fastq.gz	Fastqsanger.gz
	SRR7651693_2.fastq.gz	Fastqsanger.gz
	SRR7651694_1.fastq.gz	Fastqsanger.gz

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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage (ATAC-seq)

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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage (Whole Exome-seq)

Project description:Small cell carcinomas from different tissues exhibit transcriptional and epigenetic convergence and suggest common vulnerabilities for therapies

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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage.

Project description:The use of potent therapies inhibiting critical oncogenic pathways active in epithelial cancers has led to multiple resistance mechanisms, including the development of highly aggressive, small cell neuroendocrine carcinoma (SCNC). SCNC patients have a dismal prognosis due in part to a limited understanding of the molecular mechanisms driving this malignancy and the lack of effective treatments. Here, we demonstrate that a common set of defined oncogenic drivers reproducibly reprograms normal human prostate and lung epithelial cells to small cell prostate cancer (SCPC) and small cell lung cancer (SCLC), respectively. We identify shared active transcription factor binding regions in the reprogrammed prostate and lung SCNCs by integrative analyses of epigenetic and transcriptional landscapes. These results suggest that neuroendocrine cancers arising from distinct epithelial tissues may share common vulnerabilities that could be exploited for the development of drugs targeting SCNCs.

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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage (RNA-seq)

Project description:Small cell carcinomas from different tissues exhibit transcriptional and epigenetic convergence and suggest common vulnerabilities for therapies

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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage (ATAC-seq)

Project description:Small cell carcinomas from different tissues exhibit transcriptional and epigenetic convergence and suggest common vulnerabilities for therapies

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PARCB Project: Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage

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

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Niacin restriction with NAMPT-inhibition is synthetic lethal to neuroendocrine carcinoma (Cell NAMPTi treatment)

Project description:NAMPT plays a major role in NAD biosynthesis in many cancers and is an attractive potential cancer target. However, factors dictating therapeutic efficacy of NAMPT inhibitors (NAMPTi) are unclear. We report that neuroendocrine phenotypes predict lung and prostate carcinoma vulnerability to NAMPTi, and that NAMPTi therapy against those cancers is enhanced by dietary modification. Neuroendocrine differentiation of tumor cells was associated with down-regulation of genes relevant to QPRT-dependent de novo NAD synthesis, promoting NAMPTi susceptibility in vitro. We also found that circulating nicotinic acid riboside (NAR), a non-canonical niacin absent in culture media, antagonizes NAMPTi efficacy as it fuels NAMPT-independent but NMRK1-dependent NAD synthesis in tumors. In mouse transplantation models, depleting blood NAR by nutritional or genetic manipulations was synthetic lethal to tumors when combined with NAMPTi. Our findings provide a rationale for simultaneous targeting of NAR metabolism and NAMPT therapeutically in neuroendocrine carcinoma. Cell NAMPTi treatment is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS7251' rel='noopener noreferrer' target='_blank'>MTBLS7251</a>.Mouse NAMPT targeted therapy is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS7252' rel='noopener noreferrer' target='_blank'>MTBLS7252</a>.Mouse NAD targeted time-course is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS7253' rel='noopener noreferrer' target='_blank'>MTBLS7253</a>.

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Niacin restriction with NAMPT-inhibition is synthetic lethal to neuroendocrine carcinoma (Mouse NAMPT targeted therapy)

Project description:NAMPT plays a major role in NAD biosynthesis in many cancers and is an attractive potential cancer target. However, factors dictating therapeutic efficacy of NAMPT inhibitors (NAMPTi) are unclear. We report that neuroendocrine phenotypes predict lung and prostate carcinoma vulnerability to NAMPTi, and that NAMPTi therapy against those cancers is enhanced by dietary modification. Neuroendocrine differentiation of tumor cells was associated with down-regulation of genes relevant to QPRT-dependent de novo NAD synthesis, promoting NAMPTi susceptibility in vitro. We also found that circulating nicotinic acid riboside (NAR), a non-canonical niacin absent in culture media, antagonizes NAMPTi efficacy as it fuels NAMPT-independent but NMRK1-dependent NAD synthesis in tumors. In mouse transplantation models, depleting blood NAR by nutritional or genetic manipulations was synthetic lethal to tumors when combined with NAMPTi. Our findings provide a rationale for simultaneous targeting of NAR metabolism and NAMPT therapeutically in neuroendocrine carcinoma. Mouse NAMPT targeted therapy is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS7252' rel='noopener noreferrer' target='_blank'>MTBLS7252</a>.Cell NAMPTi treatment is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS7251' rel='noopener noreferrer' target='_blank'>MTBLS7251</a>.Mouse NAD targeted time-course is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS7253' rel='noopener noreferrer' target='_blank'>MTBLS7253</a>.

2023-10-10 | MTBLS7252 | MetaboLights

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