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HDAC in PDAC

ABSTRACT: Transcriptome analysis of murine Hdac2 knockout pancreatic tumor cells.

PROVIDER: PRJEB35204 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6594530.fastq.gz	Fastqsanger.gz
	ERR6594531.fastq.gz	Fastqsanger.gz
	ERR6594532.fastq.gz	Fastqsanger.gz
	ERR6594533.fastq.gz	Fastqsanger.gz
	ERR6594534.fastq.gz	Fastqsanger.gz

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Genome-wide chromatin binding of Hdac2 in murine PDAC cells (ChIP-Seq)

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Project description:H3K27ac ChIP-se and ATAC-seq were used to determine epigenetic differences between Hdac2 knockout versus Hdac2 wildtype pancreatic cancer cells.

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Project description:CD8+ T cells are master effectors of anti-tumor immunity and their presence at tumor sites correlates with favorable outcomes. However, metabolic constraints imposed by the tumormicroenvironment can dampen their ability to control tumor progression. We will analyze the transcriptional profile of CD8+ T cells infiltrating murine tumors during progression in a pre-cinical model pancreatic ductal adenocarcinoma (PDA).

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Project description:Pancreatic ductal adenocarcinoma (PDAC) is characterized by the presence of abundant desmoplatic stroma primarily composed of cancer-associated fibroblasts (CAFs). It is generally accepted that CAFs stimulate tumor progression and might be implicated in drug resistance and immunosuppression. Here, we have compared the transcriptional profile of PDGFRα+ CAFs isolated from genetically engineered mouse PDAC tumors with that of normal pancreatic fibroblasts (NPFs) to identify genes potentially implicated in their pro-tumorigenic properties. We report that the most differentially expressed gene, Saa3, a member of the acute-phase Serum Amyloid A (SAA) apolipoprotein family, is a key mediator of the pro-tumorigenic activity of PDGFRα+ CAFs. Whereas Saa3 competent CAFs stimulate the growth of PDAC tumor cells in an orthotopic model, Saa3 null CAFs inhibit tumor growth. Saa3 also plays a role in the cross-talk between CAFs and tumor cells. Ablation of Saa3 in pancreatic tumor cells makes them insensitive to the inhibitory effect of Saa3 null CAFs. As a consequence, germline ablation of Saa3 does not prevent PDAC tumor development in mice. The pro-tumorigenic activity of Saa3 in CAFs is mediated by Mpp6, a member of the palmitoylated membrane protein subfamily of the peripheral membrane-associated guanylate kinases. Finally, we interrogated whether these observations could be translated to a human scenario. Indeed, SAA1, the orthologue of murine Saa3, is overexpressed in human CAFs. Moreover, high levels of SAA1 in the stromal component correlate with worse survival. These findings support the concept that selective inhibition of SAA1 in CAFs may provide potential therapeutic benefit to PDAC patients.

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Genome-wide chromatin binding of Hdac2 in murine PDAC cells (ChIP-Seq)

Project description:Genome-wide chromatin binding of Hdac2 in murine PDAC cells (ChIP-Seq)

| PRJNA762060 | ENA

Genome-wide DNA methylation patterns in pancreatic ductal adenocarcinoma (PDAC)

Project description:Determine methylation pattern in PDAC a genome-wide analysis was performed in a cohort of 167 PDAC and 29 adjacent pancreatic tissues samples using the Infinium 450k methylation arrays (Illumina). 167 pancreatic tumors (PDAC) x 29 adjacent -non tumor samples.

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