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Expression Analysis of Mouse Tumor Pancreatic Ductal Adenocarcinoma (PDA) Organoids upon Spdef deletion and re-instatement

ABSTRACT: Expression Analysis of Mouse Tumor Pancreatic Ductal Adenocarcinoma (PDA) Organoids upon Spdef deletion and re-instatement

PROVIDER: PRJNA800816 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17772025_1.fastq.gz	Fastqsanger.gz
	SRR17772025_2.fastq.gz	Fastqsanger.gz
	SRR17772026_1.fastq.gz	Fastqsanger.gz
	SRR17772026_2.fastq.gz	Fastqsanger.gz
	SRR17772027_1.fastq.gz	Fastqsanger.gz

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Expression Analysis of Mouse Tumor Pancreatic Ductal Adenocarcinoma (PDA) Organoids upon Spdef deletion and re-instatement

Project description:This study used Illumina strand-specific, paired-end RNA-sequencing to examine gene expression differences following Spdef deletion and re-instatement in epithelial organoid cultures of primary tumor cells from KrasLSLG12D/+; Trp53LSLR172H/+; Pdx1-Cre (KPC) mice.

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Project description:We have carried out transcriptional profile analysis in WT MICE and bitransgenic Pdx1-cre/Kras*A MICE baring Pancreatic Ductal Adenocarcinoma Mouse models faithfully simulating human cancer are valuable for genetic identification of potential drug-targets but, among them, the most advantageous for practical use in subsequent preclinical testing of candidate therapeutic regimes are those exhibiting rapid tumor development. Considering that a KRAS mutation (predominantly in codon 12, such as KRASG12D; KRAS*) occurs with high frequency (~90%) in cases of human pancreatic ductal adenocarcinoma (PDA)1, we sought to develop a mouse PDA model that would exhibit high tumor incidence and short latency by ectopic overexpression of Kras*. Five WT mice and 6 bitransgenic Pdx1-cre/Kras*A MICE baring Pancreatic Ductal Adenocarcinoma were used to identify key genes in the formation of panceatic malignacies

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