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Links from GEO DataSets

Items: 20

1.

Enhancer reprogramming promotes pancreatic cancer progression and metastasis

(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:
GPL19057 GPL18573
136 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE99311
ID:
200099311
2.

Enhancer reprogramming promotes pancreatic cancer progression and metastasis [RNA-seq]

(Submitter supplied) Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal human malignancies, owing in part to its propensity for metastasis. Here, we used an organoid culture system to investigate how transcription and the enhancer landscape become altered during each stage of PDA progression. This approach revealed that the metastatic transition is accompanied by massive, and recurrent alterations in enhancer activity. more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL19057
36 Samples
Download data: TXT
Series
Accession:
GSE99310
ID:
200099310
3.

Enhancer reprogramming promotes pancreatic cancer progression and metastasis [ChIP-seq]

(Submitter supplied) Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal human malignancies, owing in part to its propensity for metastasis. Here, we used an organoid culture system to investigate how transcription and the enhancer landscape become altered during each stage of PDA progression. This approach revealed that the metastatic transition is accompanied by massive, and recurrent alterations in enhancer activity. more...
Organism:
Mus musculus; Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL19057
90 Samples
Download data: BIGWIG
Series
Accession:
GSE99284
ID:
200099284
4.

Enhancer reprogramming promotes pancreatic cancer progression and metastasis [ATAC-seq]

(Submitter supplied) Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal human malignancies, owing in part to its propensity for metastasis. Here, we used an organoid culture system to investigate how transcription and the enhancer landscape become altered during each stage of PDA progression. This approach revealed that the metastatic transition is accompanied by massive, and recurrent alterations in enhancer activity. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
10 Samples
Download data: BIGWIG
Series
Accession:
GSE99275
ID:
200099275
5.

Single Cell RNA seq of Genetically Engineered Mouse Models of Pancreatic Adenocarcinoma

(Submitter supplied) We report the scRNAseq profiles of three mouse models of pancreatic cancer: KIC, KPfC, KPC. Analyses demonstrate the existence of 2 molecular subtypes of cancer cells, 2 molecular subtypes of cancer associated fibroblasts, and 2 molecular subtypes of cancer associated macrophages.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
5 Samples
Download data: MTX, TSV
Series
Accession:
GSE125588
ID:
200125588
6.

Annexin A2 controls pancreatic cancer invasion and metastasis through a novel axon guidance pathway

(Submitter supplied) The mechanisms involved in promoting metastasis of pancreatic ductal adenocarcinoma have yet to be elucidated. Here, we show that AnnexinA2 regulates the secretion of Semaphorin3D from pancreatic tumor cells allowing it to bind to its receptor PlexinD1 on the surface of the tumor cell, which induces invasion and metastasis. Knockdown of AnnexinA2 or Semaphorin3D decreases the metastatic potential of pancreatic tumor cells, while over expression of AnnexinA2 or Semaphorin3D is sufficient to rescue the invasion capacity of these cells. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6096
2 Samples
Download data: CEL
Series
Accession:
GSE62285
ID:
200062285
7.

TP63-mediated enhancer reprogramming drives the squamous subtype of pancreatic ductal adenocarcinoma

(Submitter supplied) The aberrant expression of squamous lineage markers in pancreatic ductal adenocarcinoma (PDA) has been correlated with poor clinical outcomes. However, the functional role of this putative trans-differentiation event in PDA pathogenesis remains unclear. Here, we show that expression of the transcription factor TP63 (ΔN isoform) is sufficient to install and sustain the enhancer landscape and transcriptional signature of the squamous lineage in human PDA cells. more...
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL11154 GPL18573 GPL19057
92 Samples
Download data: BIGWIG
Series
Accession:
GSE115463
ID:
200115463
8.

TP63-mediated enhancer reprogramming drives the squamous subtype of pancreatic ductal adenocarcinoma (RNA-seq)

(Submitter supplied) The aberrant expression of squamous lineage markers in pancreatic ductal adenocarcinoma (PDA) has been correlated with poor clinical outcomes. However, the functional role of this putative trans-differentiation event in PDA pathogenesis remains unclear. Here, we show that expression of the transcription factor TP63 (ΔN isoform) is sufficient to install and sustain the enhancer landscape and transcriptional signature of the squamous lineage in human PDA cells. more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL11154 GPL19057
42 Samples
Download data: TXT
Series
Accession:
GSE115462
ID:
200115462
9.

TP63-mediated enhancer reprogramming drives the squamous subtype of pancreatic ductal adenocarcinoma (ChIP-seq)

(Submitter supplied) The aberrant expression of squamous lineage markers in pancreatic ductal adenocarcinoma (PDA) has been correlated with poor clinical outcomes. However, the functional role of this putative trans-differentiation event in PDA pathogenesis remains unclear. Here, we show that expression of the transcription factor TP63 (ΔN isoform) is sufficient to install and sustain the enhancer landscape and transcriptional signature of the squamous lineage in human PDA cells. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
50 Samples
Download data: BIGWIG
Series
Accession:
GSE115461
ID:
200115461
10.

BACH1 alters the expression of EMT-related genes to promote metastasis in pancreatic cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL16791 GPL17303
16 Samples
Download data: BW
Series
Accession:
GSE124408
ID:
200124408
11.

BACH1 alters the expression of EMT-related genes to promote metastasis in pancreatic cancer [RNA-seq]

(Submitter supplied) BTB and CNC homology 1 (BACH1) has been implicated in RAS-driven tumor formation. We focused on the role of BACH1 in Pancreatic ductal adenocarcinoma (PDAC), more than 90% of which have KRAS mutation. BACH1 directly or indirectly repressed the expression of genes for epithelial cell adhesion in AsPC-1 cells and SW1990. Knockdown and overexpression of BACH1 in PDAC cell lines indicated that BACH1 promoted cell migration and invasion in part by reducing E-cadherin expression.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17303
12 Samples
Download data: TXT
Series
Accession:
GSE124407
ID:
200124407
12.

BACH1 alters the expression of EMT-related genes to promote metastasis in pancreatic cancer [ChIP-Seq]

(Submitter supplied) BTB and CNC homology 1 (BACH1) has been implicated in RAS-driven tumor formation. We focused on the role of BACH1 in Pancreatic ductal adenocarcinoma (PDAC), more than 90% of which have KRAS mutation. BACH1 directly or indirectly repressed the expression of genes for epithelial cell adhesion in AsPC-1 cells and SW1990. Knockdown and overexpression of BACH1 in PDAC cell lines indicated that BACH1 promoted cell migration and invasion in part by reducing E-cadherin expression.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
4 Samples
Download data: BW
Series
Accession:
GSE124406
ID:
200124406
13.

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

(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
Series
Accession:
GSE108843
ID:
200108843
14.

Murine Pancreatic Cancer Cells: KLF10 wild type vs KLF10 knockout

(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
Series
Accession:
GSE85521
ID:
200085521
15.

SMAD4 represses FOSL1 expression and pancreatic cancer metastatic colonization

(Submitter supplied) Less than 8% of patients diagnosed with pancreatic ductal adenocarcinomas (PDAC) survive more than five years in part due to late stage diagnosis. Approximately half of PDAC patients exhibit loss of SMAD4, which correlates with increased metastatic disease. Here we demonstrate that SMAD4 is a suppressor of metastatic colonization. Using isogenic human PDAC cell lines expressing or lacking SMAD4, both in vitro and in vivo, we define SMAD4-dependent gene expression changes in metastatic lesions. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
70 Samples
Download data
16.

A mucus production programme promotes classical pancreatic ductal adenocarcinoma

(Submitter supplied) CUT&RUN for IgG, H3K4me3 and HA-SPDEF in human PDA HPAF-II cells and CUT&RUN HA-Spdef in murine KPC 2D FC1245 cells We performed CUT&RUN assay in human and murine PDA cells to profile the direct binding of SPDEF to target genes.
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL19057 GPL18573
12 Samples
Download data: BED, BW
Series
Accession:
GSE250519
ID:
200250519
17.

Expression analysis of SPDEF KO and hRosa26 clones of hF27, CFPAC1 and HPAF-II orthotopically grafted into the pancreata of NSG mice.

(Submitter supplied) This study used Illumina RNA-sequencing to examine gene expression differences following Spdef deletion in hF27, CFPAC1 and HPAF-II orthotopically grafted tumor models.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
29 Samples
Download data: RESULTS
Series
Accession:
GSE211348
ID:
200211348
18.

Single-cell analysis of murine pancreatic ductal adenocarcinoma cells reveals the transcriptional dynamics of pancreatic cancer progression..

(Submitter supplied) This study used 10X Genomics, single-cell RNA-sequencing to examine the differentiation states of cancer cells present in tumors derived from the KrasLSL-G12D; Trp53LSL-R172H; Pdx1-Cre (KPC) mouse model of pancreatic ductal adenocarcinoma. The study analyzed tumors from 8 different mice.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: CSV, H5, RDS
Series
Accession:
GSE195914
ID:
200195914
19.

Expression Analysis of Mouse Tumor Pancreatic Ductal Adenocarcinoma (PDA) Organoids upon Spdef deletion and re-instatement

(Submitter supplied) This study used Illumina strand-specific, paired-end RNA-sequencing to examine gene expression differences following Spdef deletion and re-instatement in epithelial organoid cultures of primary tumor cells from KrasLSLG12D/+; Trp53LSLR172H/+; Pdx1-Cre (KPC) mice.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
12 Samples
Download data: RESULTS
Series
Accession:
GSE195502
ID:
200195502
20.

RNA-Seq Samples of siTFE3 in 8988T PDA Cell Line to Investigate Transcriptional Control of the Autophagy-Lysosome System

(Submitter supplied) The activation of cellular quality control pathways to maintain metabolic homeostasis and mitigate diverse cellular stresses is emerging as a critical growth and survival mechanism in many cancers. Autophagy, a highly conserved cellular self-degradative process, is a key player in the initiation and maintenance of pancreatic ductal adenocarcinoma (PDA). However, the regulatory circuits that activate autophagy, and how they enable reprogramming of PDA cell metabolism are unknown. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: FPKM_TRACKING
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