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E-GEOD-51786

ABSTRACT: Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [array]

OTHER RELATED OMICS DATASETS IN: PRJNA227370PRJNA227898PRJNA225023

TISSUE(S): Not Specified, Liver, Kidney

PROVIDER: E-GEOD-51786 | ExpressionAtlas | 2015-07-27

REPOSITORIES: ExpressionAtlas

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Dataset's files

Source:

			Action	DRS
	E-GEOD-51786-analysis-methods.tsv	Tabular
	E-GEOD-51786-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-51786-configuration.xml	Xml
	E-GEOD-51786-percentile-ranks.tsv	Tabular
	E-GEOD-51786.condensed-sdrf.tsv	Tabular

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Project description:Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [array]

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Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation

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Dynamic partitioning of branched-chain amino acids-derived nitrogen supports renal cancer progression

Project description:<p>Metabolic reprogramming is critical for tumor initiation and progression. However, the exact impact of specific metabolic changes on cancer progression is poorly understood. Here, we integrate multimodal analyses of primary and metastatic clonally-related clear cell renal cancer cells (ccRCC) grown in physiological media to identify key stage-specific metabolic vulnerabilities. We show that a VHL loss-dependent reprogramming of branched-chain amino acid catabolism sustains the de novo biosynthesis of aspartate and arginine enabling tumor cells with the flexibility of partitioning the nitrogen of the amino acids depending on their needs. Importantly, we identify the epigenetic reactivation of argininosuccinate synthase (ASS1), a urea cycle enzyme suppressed in primary ccRCC, as a crucial event for metastatic renal cancer cells to acquire the capability to generate arginine, invade in vitro and metastasize in vivo. Overall, our study uncovers a novel mechanism of metabolic flexibility occurring during ccRCC progression, paving the way for the development of novel stage-specific therapies</p>

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Epigenetic reprogramming shapes the cellular landscape of schwannoma

Project description:Cell state evolution underlies tumor development and response to therapy1, but mechanisms specifying cancer cell states and intratumor heterogeneity are incompletely understood. Schwannomas are the most common tumors of the peripheral nervous system and are treated with surgery and ionizing radiation2–5. Schwannomas can oscillate in size for many years after radiotherapy6,7, suggesting treatment may reprogram schwannoma cells or the tumor microenvironment. Here we show epigenetic reprogramming shapes the cellular landscape of schwannomas. We find schwannomas are comprised of 2 molecular groups distinguished by reactivation of neural crest development pathways or misactivation of nerve injury mechanisms that specify cancer cell states and the architecture of the tumor immune microenvironment. Schwannoma molecular groups can arise independently, but ionizing radiation is sufficient for epigenetic reprogramming of neural crest to immune-enriched schwannoma by remodeling chromatin accessibility, gene expression, and metabolism to drive schwannoma cell state evolution and immune cell infiltration. To define functional genomic mechanisms underlying epigenetic reprograming of schwannomas, we develop a technique for simultaneous interrogation of chromatin accessibility and gene expression coupled with genetic and therapeutic perturbations in single-nuclei. Our results elucidate a framework for understanding epigenetic drivers of cancer evolution and establish a paradigm of epigenetic reprograming of cancer in response to radiotherapy.

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Purinergic Preconditioning Induces Epigenomic and Transcriptomic Changes Resembling Epilepsy-associated Microglial States

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