GEO DataSets

(Submitter supplied) Aldh1b1 expressing, adult mouse pancreatic stem cells, were isolated and subjected to single cell RNA Seq. 

Organism:

synthetic construct; Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL17021 GPL19604

856 Samples

Download data: TSV

(Submitter supplied) Mouse embryonic pancreata at 14.5 dpc were cultured for two day in air to liquide interface cultures in the absence (control) or presence of 10 uM AMI-5, a protein methyltransferase inhibitor

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL17021 GPL19057

6 Samples

Download data: TXT

(Submitter supplied) In this dataset, we include the expression data obtained from KRas expressing tumors, matched Kras expressing tumor spheres, surviving cells and surviving cells after KRas re-expression for 24hs

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

20 Samples

Download data: CEL

(Submitter supplied) We have previously described in mouse models that pancreas-specific deletion of Gata6 results in pancreas alterations by rendering pancreatic acinar cells in a non-fully differentiation state, and furthermore it accelerates tumor initiation and progression in a pro-tumorigenic context (KrasG12V expression). We aim to determine the sites where Gata6 binds at the genome-wide level in the pancreas to unveil why its loss leads to altered pancreatic function and enhanced tumor formation when coexpressed with KrasG12V.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11002

5 Samples

Download data: BED, WIG

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

Organism:

Mus musculus; Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL11002 GPL10999

10 Samples

Download data: TXT, WIG

(Submitter supplied) We report the global gene expression of mouse pancreatic cells in a pancreas-specific conditional knock-out mouse for Gata6, as compared with age-matched controls. Total RNA was extracted from the pancreas of 6-8 -week old mice of the two genotypes and analyzed. at this age, Gata6P-/- pancreata are histologically normal, but the acinar differentiation programme is already altered. we observe that loss of Gata6 causes the de-repression of ectopic non-pancreatic genes, as well as some genes involved in the mesenchymal programme.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11002

8 Samples

Download data: TXT

(Submitter supplied) By studying a mouse model, as well as human tumors samples and cell lines, we have revealed a tumor suppressive role for Gata6 in the pathogenesis of pancreatic ductal adenocarcinoma (PDAC). In order to understand the mechanism underlying such tumor suppressive function, we analyzed the genome-wide DNA-binding of GATA6 in a human PDAC cell line (PaTu8988S). GATA6 is found to bind the promoter of genes involved in the epithelial differentiation programme, as well as of genes involved in the mesenchymal programme. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL10999

2 Samples

Download data: TXT, WIG

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

Organism:

Mus musculus

Type:

Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL19057 GPL6246

22 Samples

Download data: BW, CEL

(Submitter supplied) Accumulation of genetic mutations is thought to be a primary cause of cancer. However, a set of genetic mutations sufficient for cancer development remains unclear in most cancers, including pancreatic cancer. Here, we examined the effect of in vivo reprogramming on Kras-induced cancer development. We first demonstrate that Kras and p53 mutations are insufficient to induce activation of ERK signaling and cancer development in the pancreas. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

14 Samples

Download data: BW

(Submitter supplied) Accumulation of genetic mutations is thought to be a primary cause of cancer. However, a set of genetic mutations sufficient for cancer development remains unclear in most cancers, including pancreatic cancer. Here, we examined the effect of in vivo reprogramming on Kras-induced cancer development. We first demonstrate that Kras and p53 mutations are insufficient to induce activation of ERK signaling and cancer development in the pancreas. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

8 Samples

Download data: CEL

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

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL18573 GPL19057

12 Samples

Download data: BW

(Submitter supplied) ARID1A restrains the formation of PanIN, pancreas ductal adenocarcinoma, and intraductal mucinous neoplasms

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

4 Samples

Download data: BW

(Submitter supplied) ARID1A restrains the formation of PanIN, pancreas ductal adenocarcinoma, and intraductal mucinous neoplasms

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

8 Samples

Download data: TXT

(Submitter supplied) We identified miR-21 and miR-224 as cell-specific and compartment-specific regulators in PanINs and PDA. miR-21 is overexpressed in tumor epithelial cells of premalignant ducts, while miR-224 is overexpressed in cancer-associated fibroblasts in PDA stroma. Inhibition of miR-21 reverted pro-tumorigenic functionalities to baseline levels. Overexpression of miR-224 induced activated phenotypes in normal fibroblasts. more...

Organism:

Mus musculus; Rattus norvegicus

Type:

Expression profiling by RT-PCR

Platform:

GPL22525

21 Samples

Download data: TXT

(Submitter supplied) We identified miR-21 and miR-224 as cell-specific and compartment-specific regulators in PanINs and PDA. miR-21 is overexpressed in tumor epithelial cells of premalignant ducts, while miR-224 is overexpressed in cancer-associated fibroblasts in PDA stroma. Inhibition of miR-21 reverted pro-tumorigenic functionalities to baseline levels. Overexpression of miR-224 induced activated phenotypes in normal fibroblasts. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

8 Samples

Download data: TXT, XLSX

(Submitter supplied) The objective of this study was to elucidate the role of Nupr1 in pancreatic tumorigenesis. Using the Pdx-1-cre;LSL-KrasG12D mouse as model we discovered that, in contrast to KrasG12D pancreas that develop multiple foci of pancreatic intraepithelial neoplasia (PanIN), KrasG12D;Nupr1KO pancreas were free from such lesions, indicating that Nupr1 is pivotal for PanIN formation. In vitro, MiaPaCa2 cells activated Nupr1 expression in response to nutrient deprivation and this expression was necessary for cell survival. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

14 Samples

Download data: CEL

(Submitter supplied) Pancreatic cancer is characterized by heavy desmoplasia. Triptolide and its water-soluble pro-drug Minnelide are extremely efficient against pancreatic cancer in animal models. However, the effects of triptolide on pancreatic cancer stromal cells are largely unknown. The aim of this project is to indentify potential cellular functions that are affected by triptolide in pancreatic cancer associated fibroblasts.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

9 Samples

Download data: TXT

(Submitter supplied) Immune evasion is a hallmark of KRAS-driven cancers, but underlying mechanism and clinical implications remain unclear.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

8 Samples

Download data: CSV

(Submitter supplied) We used CRISPR/Cas9 genome editing to inactivate KRAS in pancreatic cancer cells and isolated cell populations that still produce tumors in mice. We show that the malignant phenotype of KRAS knockout cells is stable. However, KRAS deficient cancer cells fail to avoid detection and elimination by the host immune system, indicating that a key aspect of tumor maintenance by oncogenic KRAS is to promote immune evasion. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

3 Samples

Download data: MTX, TSV

(Submitter supplied) 5-methylcytosine sites of mRNA in BxPC-3, PANC1, and MiaPaCa-2 pancreatic cancer cells at the single-base resolution by whole-transcriptome bisulfite sequencing.

Organism:

Homo sapiens

Type:

Methylation profiling by high throughput sequencing; Other

Platform:

GPL18573

15 Samples

Download data: XLSX