GEO DataSets

Analysis of primary pancreatic ductal epithelial cells (PDECs) established from 6-week-old Pdx1-Cre;LSL-KrasG12D L/+;Pten L/+ animals. Oncogenic KrasG12D and Pten deficiency cooperate to induce pancreatic ductal adenocarcinoma (PDAC). Results provide insight into molecular basis of PDAC development.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE25828

8 Samples

Download data: CEL

(Submitter supplied) Almost all human pancreatic ductal adenocarcinomas (PDACs) are driven by oncogenic Kras and the progression of the disease is characterized by the serial appearance of certain genetic lesions. Mouse models have convincingly shown that Kras mutation induces classical PanIN lesions that can progress to PDAC in the appropriate tumor suppressor background. However, the cooperative mechanism between mutant Kras-dependent signaling surrogates and other oncogenic pathways remains to be fully elucidated in order to devise better therapeutic strategy. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4528

Platform:

GPL1261

8 Samples

Download data: CEL

(Submitter supplied) That mutational activation of Kras and inactivation of p16 are two signature genetic alterations required for development of PDAC. To elucidate the downstream pathways activated by oncogenic Kras and inactivated p16 in human pancreatic tumorigenesis, we profiled gene expression in HPNE/Kras/shp16 and HPNE/Kras cells using cDNA microarray analysis.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

1 Sample

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by array

Platforms:

GPL4134 GPL6246

13 Samples

Download data: CEL, TXT

(Submitter supplied) 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.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

12 Samples

Download data: CEL

(Submitter supplied) Constitutive Kras and NF-kappaB activation is identified as signature alterations in human pancreatic ductal adenocarcinoma (PDAC). However, the mechanisms of constitutive NF-kappaB activation in KrasG12D-induced PDAC are not yet understood. Here, we report that pancreas-targeted IKK2/beta inactivation inhibited NF-kappaB activation and completely suppressed PDAC development in KrasG12D and KrasG12D;Ink4a/Arf mutant mice, demonstrating a genetic link between IKK2/beta and KrasG12D in PDAC inception. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL4134

1 Sample

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by array; Genome variation profiling by genome tiling array

Platforms:

GPL24320 GPL6887 GPL15076

132 Samples

Download data: TXT

(Submitter supplied) Primary cell cultures were isolated from different KrasG12D-driven mouse models of pancreatic cancers and subjected to array comparative genomic hybridization (aCGH) for the investigation of copy number profiles.

Organism:

Mus musculus

Type:

Genome variation profiling by genome tiling array

Platforms:

GPL15076 GPL24320

115 Samples

Download data: TXT

(Submitter supplied) Primary cell cultures were isolated from KrasG12D-driven, PiggyBac transposon-transposase pancreatic cancer cell cultures and subjected to microarray-based expression profiling for the investigation of expression profiles.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6887

17 Samples

Download data: TXT

(Submitter supplied) Objective Oncogenic Kras-activated robust Mek/Erk signals phosphorylate to the tuberous sclerosis complex (Tsc) and deactivates mammalian target of rapamycin (mTOR) suppression in pancreatic ductal adenocarcinoma (PDAC); however, Mek and mTOR inhibitors alone have demonstrated minimal clinical antitumor activity. Design We generated transgenic mouse models in which mTOR was hyperactivated either through the Kras/Mek/Erk cascade, by loss of Pten or through Tsc1 haploinsufficiency. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

22 Samples

Download data: CEL

(Submitter supplied) 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.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

4 Samples

Download data: CEL

(Submitter supplied) Transcriptional profiling of mouse pancreatic cancer cells comparing Pdx-1Cre LSL-KrasG12D P53L/L cells with Pdx-1Cre LSL-KrasG12D KLF10L/L P53L/L cells, and to determine the effects of KLF10 deficiency on murine PDAC gene expression.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL10787

3 Samples

Download data: TXT, XLS

(Submitter supplied) We report single cell RNA sequencing of pancreatic enzymatically digested whole, fresh tumors from a genetically engineered mouse model (GEMM) of pancreatic adenocarcinoma. This GEMM consists of pancreas specific expression of oncogenic Kras (Kras-G12D) in addition of homozygous deletion of the ring finger domain (catalytic domain) of Rnf43. This GEMM is termed 'KRC'.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

10 Samples

Download data: TAR

(Submitter supplied) This project describes the establishment and validation of a murine orthotopic xenograft model using fresh human tumor samples that recapitulates the critical components of human pancreatic adenocarcinoma. The authors discuss the proven and theoretical advantages of the model as well as future translational implications. Background: Relevant preclinical models that recapitulate the key features of human pancreatic ductal adenocarcinoma (PDAC) are needed in order to provide biologically tractable models to probe disease progression and therapeutic responses and ultimately improve patient outcomes for this disease. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

47 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

41 Samples

Download data: CEL

(Submitter supplied) Activating mutations in KRAS are among the most frequent events in diverse human carcinomas and are particularly prominent in human pancreatic ductal adenocarcinoma (PDAC). An inducible KrasG12D-driven mouse model of PDAC has established a critical role for sustained KrasG12D expression in tumor maintenance, providing a model to determine the potential for, and underlying mechanisms of, KrasG12D–independent PDAC recurrence. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

5 Samples

Download data: CEL

(Submitter supplied) Activating mutations in KRAS are among the most frequent events in diverse human carcinomas and are particularly prominent in human pancreatic ductal adenocarcinoma (PDAC). An inducible KrasG12D-driven mouse model of PDAC has established a critical role for sustained KrasG12D expression in tumor maintenance, providing a model to determine the potential for, and underlying mechanisms of, KrasG12D–independent PDAC recurrence. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

36 Samples

Download data: CEL

(Submitter supplied) Cyclooxygenase-2 (COX-2) is upregulated in pancreatic ductal adenocarcinomas (PDAC). However, how COX-2 promotes PDAC development is unclear. While previous studies have evaluated the efficacy of COX-2 inhibition via the use of non steroidal anti-inflammatory drugs (NSAIDs) or the COX-2 inhibitor celecoxib in PDAC models, none have addressed the cell intrinsic vs. microenvironment roles of COX-2 in modulating PDAC initiation and progression. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4338

Platform:

GPL1261

8 Samples

Download data: CEL

Analysis of PDACs from mutants with pancreatic-specific Pten loss (Pten +/-) and K-ras activation (K-rasG12D) and either COX-2 over-expression (Cox-2 COE) or knockout (Cox-2 KO) under regulation of the Pdx-1 promoter. Results provide insight into the role of COX-2 in pancreatic cancer development.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE38988

8 Samples

Download data: CEL

(Submitter supplied) Nuclear Protein 1 (Nupr1) is a major actor of the cell stress response required for KrasG12D-driven formation of pancreatic intraepithelial neoplastic (PanINs) lesions in mice. We investigated the impact of Nupr1-depletion on the development and biology of murin pancreatic adenocarcinomas (PDAC) in the Pdx1-cre;LSL-KrasG12D;Ink4a/Arffl/fl (KIC) mice. We found that only one half of Nupr1-deficient mice developed PDAC. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

7 Samples

Download data: CEL