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Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [ChIP-seq]

ABSTRACT: Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [ChIP-seq]

PROVIDER: PRJNA747009 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15164742.fastq.gz	Fastqsanger.gz
	SRR15164743.fastq.gz	Fastqsanger.gz
	SRR15164744.fastq.gz	Fastqsanger.gz

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Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis

Project description:Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis

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Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [RNA-seq]

Project description:Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [RNA-seq]

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Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [scRNA-Seq]

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Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [RNA-seq]

Project description:Inflammation is a major risk factor for pancreatic ductal adenocarcinoma (PDAC). When occurring in the context of pancreatitis, mutations of KRAS accelerate tumor development. We discovered that long after its complete resolution, a transient inflammatory event primes pancreatic epithelial cells to subsequent transformation by oncogenic KRAS. Upon recovery from acute inflammation, epithelial cells of the pancreas display an enduring adaptive response associated with sustained transcriptional and epigenetic reprogramming. Such adaptation enables the prompt reactivation of acinar-to-ductal metaplasia (ADM) upon subsequent inflammatory events, thus efficiently limiting tissue damage via rapid decrease of zymogen production. We propose that since activating mutations of KRAS maintain an irreversible ADM, they may be beneficial and under strong positive selection in the context of recurrent pancreatitis.

2021-09-17 | GSE180211 | GEO

Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [ChIP-seq]

2021-09-17 | GSE180199 | GEO

Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [scRNA-Seq]

2021-09-17 | GSE181276 | GEO

Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [ATAC-seq]

2021-09-17 | GSE180192 | GEO

Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis

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

2021-09-17 | GSE180212 | GEO

Epithelial memory of inflammation limits tissue damage while promoting pancreatic tumorigenesis.

Project description:Inflammation is a major risk factor for pancreatic ductal adenocarcinoma (PDAC). When occurring in the context of pancreatitis, KRAS mutations accelerate tumor development in mouse models. We report that long after its complete resolution, a transient inflammatory event primes pancreatic epithelial cells to subsequent transformation by oncogenic KRAS. Upon recovery from acute inflammation, pancreatic epithelial cells display an enduring adaptive response associated with sustained transcriptional and epigenetic reprogramming. Such adaptation enables the reactivation of acinar-to-ductal metaplasia (ADM) upon subsequent inflammatory events, thereby limiting tissue damage through a rapid decrease of zymogen production. We propose that because activating mutations of KRAS maintain an irreversible ADM, they may be beneficial and under strong positive selection in the context of recurrent pancreatitis.

| S-EPMC9733946 | biostudies-literature

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