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Mus musculus

ABSTRACT: PDX1 dynamically regulates pancreatic ductal adenocarcinoma initiation and maintenance [ChIP-seq batch2]

PROVIDER: PRJNA356752 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5088682.fastq.gz	Fastqsanger.gz
	SRR5088683.fastq.gz	Fastqsanger.gz

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Gene expression analysis between the pancreatic tissues of Pdx1-cre;Kras LSL-G12D and Pdx-cre;KrasLSL-G12D;IKK2/beta F/F mice

Project description:Constitutive Kras and NF-kB activation is identified as signature alterations in human pancreatic ductal adenocarcinoma (PDAC). Here, we report that pancreas-targeted IKK2/beta inactivation inhibited NF-kB activation and completely suppressed PDAC development. Our findings demonstrated that NF-kB is required for development of pancreatic ductal adenocarcinoma that was initiated by Kras activation. Pancreatic tissue from 4 groups of mice were used in this project: (1) the pancreas normal appearance of Pdx1-cre;KrasLSL-G12D;IKK2/beta mice, (2) the normal pancreas of Pdx1-cre;KrasLSL-G12D mice, (3) the pancreatic lesion of pancreatic intraepithelial neoplasia (PanIN) of Pdx1-cre;KrasLSL-G12D mice, and (4) the pancreatic lesion of PDAC of Pdx1-cre;KrasLSL-G12D mice. Each group included three mice. RNA samples from mouse pancreas were hybridized on GeneChip Mouse Gene 1.0 ST arrays (Affymetrix). Group (1) and group (2) were compared, and group (2), group (3) and group (4) were compared.

2012-01-24 | E-GEOD-33322 | biostudies-arrayexpress

Expression data from WT mice and bitransgenic Pdx1-cre/Kras*A mice bearing Pancreatic Ductal Adenocarcinoma

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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Differential gene expression in EpCAM+ pancreatic cancer cells with Lifr deficiency

Project description:The goal of this study is to investigate the molecular mechanisms of LIFR signaling in pancreatic cancer cells isolated from the classical pancreatic ductal adenocarcinoma mouse model KrasLSL-G12D;Tp53f/f;Rosa26LSL-Luc;Pdx1-Cre mice EpCAM+ pancreatic cancer cells were isolated by FACS from pancreatic tumors developed in Lifrf/f;KrasLSL-G12D/+;Trp53f/f;Rosa26LSL-Luc;Pdx1-Cre or LifrWT;KrasLSL-G12D/+;Trp53f/f;Rosa26LSL-Luc;Pdx1-Cre mice respectively and directly lysed for RNA extraction

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In vivo response of EpCAM+ pancreatic cancer cells to gemcitabine plus anti-LIF neutralizing antibody treatment

Project description:The goal of this study is to investigate the molecular mechanisms of LIF action on pancreatic cancer cells in the classical pancreatic ductal adenocarcinoma mouse model KrasLSL-G12D;Tp53f/f;Rosa26LSL-Luc;Pdx1-Cre mice EpCAM+ pancreatic cancer cells were isolated from pancreatic tumors developped in KrasLSL-G12D;Tp53f/f;Rosa26LSL-Luc;Pdx1-Cre mice treated with either gemcitabine plus control IgG or gemcitabine plus anti-LIF antibody by FACS

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