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Effect of Notch4 deletion on pancreatic tumorigenesis in mice

ABSTRACT: The gene expression of N4-/-PKC (Notch4 -/-; p16fl/fl;LSL-KrasG12D;p48-Cre) mouse pancreatic tumor cell lines was compared to that of PKC ( p16fl/fl; LSL-KrasG12D;p48-Cre) mouse pancreatic tumor cell lines

ORGANISM(S): Mus musculus

PROVIDER: GSE184060 | GEO | 2023/03/20

REPOSITORIES: GEO

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Pancreatic tissue of 9 week old mice with genotypes Ptf1a-Cre;LSL-KrasG12D and Ptf1a-Cre;LSL-KrasG12D;Ptpn11fl/fl

Project description:To investigate the role of SHP2 (Ptpn11) in pancreatic carcinogenesis, murine pancreatic whole tissue RNA samples of 9 week old mice with the genotypes Ptf1a-Cre;LSL-KrasG12D (ID-labels Kxxx) and Ptf1a-Cre;LSL-KrasG12D;Ptpn11fl/fl (ID-labels Mxxxx) were analyzed by microarray.

2018-03-30 | E-MTAB-6399 | biostudies-arrayexpress

Pancreatic cancer-induced cachexia syndrome

Project description:Cancer cachexia syndrome is observed in 80% of patients with advanced-stage cancer, and it is one of the most frequent causes of death. Severe wasting accounts for more than 80% in patients with advanced pancreatic cancer. Here we wanted to define, by using an microarray approach and the Pdx1-cre;LSL-KrasG12D;INK4a/arffl/fl, the pathways involved in muscle, liver and white adipose tissue wasting. The aim of our work was to characterize as extensively as possible the pathways activated by the pancreatic cancer-induced cachectic tissues. For this purpose, we generated and compared genome-wide expression profiles of white adipose tissue, skeletal muscle and liver, from Pdx1-cre;LSL-KrasG12D;INK4a/arffl/fl and LSL-KrasG12D;INK4a/arffl/fl mice at 10 weeks-old. Tissue samples by triplicate was obtained from liver, muscle and adipose tissues in both groups, controls and cachectic mice. Total RNA samples was processed and profiled on Affymetrix Mouse Gene 1.0 ST arrays as previously described (Cano et al, 2012)

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Project description:Single-cell RNA sequencing analysis was performed on primary pancreatic ductal adenocarcinoma derrived cell line from PiKP (P48-Cre; R26-rtTa-IRES-EGFP; tetO-LSL-KrasG12D/+; Trp53L/L) murine tumors. In this study we establish that oncogenic Kras is the predominant driver of T cell paucity and myeloid infiltration in the pancreatic tumor microenvironment. Then, we use scRNA seq analysis of cultured PiKP cells with and without Kras* extinction to identify immune related genes involved in driving Kras* mediated immune supression in PDAC.

2023-07-22 | GSE201887 | GEO

TGIF1 loss contributes to progression of KRASG12D-induced pancreatic ductal adenocarcinoma involving HAS2-CD44 activation and PD-L1 upregulation.

Project description:Transcriptional profiling of mouse Pancreatic cancer cells comparing Pdx1-Cre LSL-KrasG12D TGIF1L/L P53L/L cells with Pdx1-Cre LSL-KrasG12D P53L/L cells, and to determine the effects of TGIF1 deletion on PDAC gene expression.

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E-MTAB-6399

Project description:Pancreatic tissue of 9 week old mice with genotypes Ptf1a-Cre;LSL-KrasG12D and Ptf1a-Cre;LSL-KrasG12D;Ptpn11fl/fl

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Pancreatic cancer-induced cachexia syndrome

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Nuclear protein (Nupr)-1 is required for pancreatic adenocarcinoma development in Pdx1-cre;LSL-KrasG12D;Ink4a/Arffl/fl mice

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2018-03-20 | MSV000082186 | MassIVE

Differential expression gene signature between primary tumors and metastatic tumors in PDAC and BC mouse models devoid of stromal contamination [GFP Sorted Cells RNA-Seq]

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