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Links from GEO DataSets

Items: 20

1.

In vivo reprogramming drives Kras-induced cancer development

(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
Series
Accession:
GSE100842
ID:
200100842
2.

In vivo reprogramming drives Kras-induced cancer development [ChIP-seq]

(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
Series
Accession:
GSE100841
ID:
200100841
3.

In vivo reprogramming drives Kras-induced cancer development [expression]

(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
Series
Accession:
GSE100840
ID:
200100840
4.

Genome-wide map of Gata6 DNA binding in mouse pancreas

(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
Series
Accession:
GSE57090
ID:
200057090
5.

Gata6

(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
Series
Accession:
GSE47537
ID:
200047537
6.

Global gene expression in the adult Gata6 null mouse pancreas

(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
Series
Accession:
GSE47536
ID:
200047536
7.

Genome-wide map of GATA6 DNA binding in human PDAC cells

(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
Series
Accession:
GSE47535
ID:
200047535
8.

Prox1 haploinsufficiency sensitizes the pancreas to KrasG12D-induced transformation

(Submitter supplied) Oncogenic mutations in Kras initiate neoplastic transformation in the pancreas through a process that hijacks the activity of developmental regulators and induces an inflammatory microenvironment. We report that the homeodomain transcription factor Prox1 is a novel component of a progenitor signature that is activated in acinar cells undergoing dedifferentiation and ductal metaplasia conversion. Also, the conditional deletion of a single Prox1 allele markedly accelerates early transformation and significantly enhances features of inflammation in pancreatic tissues carrying a Kras oncogene. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL11180
9 Samples
Download data: CEL
Series
Accession:
GSE64319
ID:
200064319
9.

Prox1 haploinsufficiency sensitizes the pancreas to KrasG12D-induced transformation

(Submitter supplied) Oncogenic mutations in Kras initiate neoplastic transformation in the pancreas through a process that hijacks the activity of developmental regulators and induces an inflammatory microenvironment. We report that the homeodomain transcription factor Prox1 is a novel component of a progenitor signature that is activated in acinar cells undergoing dedifferentiation and ductal metaplasia conversion. Also, the conditional deletion of a single Prox1 allele markedly accelerates early transformation and significantly enhances features of inflammation in pancreatic tissues carrying a Kras oncogene. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL15207
6 Samples
Download data: CEL
Series
Accession:
GSE58547
ID:
200058547
10.

Single cell transcriptomes of pancreatic pre-invasive lesions and cancer reveal acinar metaplastic cells’ heterogeneity

(Submitter supplied) In this project we have used single cell RNA-seq to profile pancreatic cancer development in a mouse model, from pre-invasive stage to cancer, and in human PDAC sample. Using a reporter gene, we were able to dissect metaplastic acinar cell heterogeneity, profiled six different acinar metaplastic cell types and states, validated their localization to pre-invasive lesions and correlated findings with human PDAC. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL16791 GPL17021
12 Samples
Download data: CSV, TXT
Series
Accession:
GSE141017
ID:
200141017
11.

RBPJ deficiency sensitizes pancreatic acinar cells to Kras-mediated PanIN initiation

(Submitter supplied) Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis and is among the most common causes of cancer death worldwide. KrasG12D mutation is the main driver mutation but insuffi-cient for progression of invasive cancer on its own indicating that other pathways, such as Notch signaling may participate in that process. RBPJ, the only transcription factor in Notch signaling, is frequently lost in human cancers and associated with more aggressive breast cancer phenotype. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
30 Samples
Download data: TXT
Series
Accession:
GSE189756
ID:
200189756
12.

Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [scRNA-Seq]

(Submitter supplied) Inflammation is a major risk factor for pancreatic ductal adenocarcinoma (PDAC). When occurring in the context of pancreatitis, mutations of KRAS accelerate tumor development. We discovered that long after its complete resolution, a transient inflammatory event primes pancreatic epithelial cells to subsequent transformation by oncogenic KRAS. Upon recovery from acute inflammation, epithelial cells of the pancreas display an enduring adaptive response associated with sustained transcriptional and epigenetic reprogramming. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: TXT
Series
Accession:
GSE181276
ID:
200181276
13.

Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
21 Samples
Download data: BED, BW, NARROWPEAK
Series
Accession:
GSE180212
ID:
200180212
14.

Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [RNA-seq]

(Submitter supplied) Inflammation is a major risk factor for pancreatic ductal adenocarcinoma (PDAC). When occurring in the context of pancreatitis, mutations of KRAS accelerate tumor development. We discovered that long after its complete resolution, a transient inflammatory event primes pancreatic epithelial cells to subsequent transformation by oncogenic KRAS. Upon recovery from acute inflammation, epithelial cells of the pancreas display an enduring adaptive response associated with sustained transcriptional and epigenetic reprogramming. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
7 Samples
Download data: TXT
Series
Accession:
GSE180211
ID:
200180211
15.

Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [ChIP-seq]

(Submitter supplied) Inflammation is a major risk factor for pancreatic ductal adenocarcinoma (PDAC). When occurring in the context of pancreatitis, mutations of KRAS accelerate tumor development. We discovered that long after its complete resolution, a transient inflammatory event primes pancreatic epithelial cells to subsequent transformation by oncogenic KRAS. Upon recovery from acute inflammation, epithelial cells of the pancreas display an enduring adaptive response associated with sustained transcriptional and epigenetic reprogramming. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
3 Samples
Download data: BED
Series
Accession:
GSE180199
ID:
200180199
16.

Epithelial memory of resolved inflammation limits tissue damage while promoting pancreatic tumorigenesis [ATAC-seq]

(Submitter supplied) Inflammation is a major risk factor for pancreatic ductal adenocarcinoma (PDAC). When occurring in the context of pancreatitis, mutations of KRAS accelerate tumor development. We discovered that long after its complete resolution, a transient inflammatory event primes pancreatic epithelial cells to subsequent transformation by oncogenic KRAS. Upon recovery from acute inflammation, epithelial cells of the pancreas display an enduring adaptive response associated with sustained transcriptional and epigenetic reprogramming. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL21103 GPL21273
7 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE180192
ID:
200180192
17.

Single cell RNA-Seq of adult mouse pancreatic stem cells and early progenitors

(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
Series
Accession:
GSE110283
ID:
200110283
18.

SWI/SNF component ARID1A restrains pancreatic neoplasia formation

(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:
GPL19057 GPL18573
12 Samples
Download data: BW
Series
Accession:
GSE119859
ID:
200119859
19.

SWI/SNF component ARID1A restrains pancreatic neoplasia formation [ChIP-seq]

(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
Series
Accession:
GSE119858
ID:
200119858
20.

SWI/SNF component ARID1A restrains pancreatic neoplasia formation [RNA-seq]

(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
Series
Accession:
GSE119779
ID:
200119779
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