Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA475105 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7276330.fastq.gz	Fastqsanger.gz
	SRR7276340.fastq.gz	Fastqsanger.gz
	SRR7276350.fastq.gz	Fastqsanger.gz
	SRR7276360.fastq.gz	Fastqsanger.gz
	SRR7276370.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 92

Similar Datasets

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

Project description: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. In addition, we demonstrate that TP63-driven enhancer reprogramming promotes aggressive tumor phenotypes, including enhanced cell motility and invasion and an accelerated growth of primary PDA tumors and metastases in vivo. Conversely, we provide evidence that squamous PDA remains addicted to TP63 to sustain the growth of primary tumors and metastases. Taken together, our study validates the functional significance of squamous trans-differentiation in PDA, and reveals TP63-based reprogramming of PDA cells as an experimental tool for investigating vulnerabilities linked to this cell fate transition.

2018-11-13 | GSE115463 | GEO

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

2018-11-13 | GSE115462 | GEO

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

2018-11-13 | GSE115461 | GEO

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

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

| PRJNA475111 | ENA

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

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

| PRJNA475110 | ENA

TP63-Mediated Enhancer Reprogramming Drives the Squamous Subtype of Pancreatic Ductal Adenocarcinoma.

Project description: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 transdifferentiation event in PDA pathogenesis remains unclear. Here, we show that expression of the transcription factor TP63 (?Np63) is sufficient to install and sustain the enhancer landscape and transcriptional signature of the squamous lineage in human PDA cells. We also demonstrate that TP63-driven enhancer reprogramming promotes aggressive tumor phenotypes, including enhanced cell motility and invasion, and an accelerated growth of primary PDA tumors and metastases in vivo. This process ultimately leads to a powerful addiction of squamous PDA cells to continuous TP63 expression. Our study demonstrates the functional significance of squamous transdifferentiation in PDA and reveals TP63-based reprogramming as an experimental tool for investigating mechanisms and vulnerabilities linked to this aberrant cell fate transition.

| S-EPMC6296757 | biostudies-literature

Pancreatic ductal adenocarcinoma

Project description:Pancreatic ductal adenocarcinoma

| PRJNA432344 | ENA

Gene expression in pancreatic ductal adenocarcinoma

Project description:To further develop our understanding of the gene expression signature of pancreatic ductal adenocarcinoma Gene expression signatures in macrodissected resected pancreatic ductal adenocarcinoma specimens

2014-03-14 | E-GEOD-55643 | biostudies-arrayexpress

Digital spatial profiling of pancreatic ductal adenocarcinoma, acinar ductal metaplasia and adjacent normal pancreas tissue

Project description:Pancreatic ductal adenocarcinoma (PDAC) is the most important histological subtype of pancreatic cancer, accounting for approximately 90% of all pancreatic cancers.Acinar to ductal metaplasia (ADM) is a recently recognized, yet less well-studied, precursor lesion of PDAC developed in the setting of chronic pancreatitis. Through digital spatial mRNA profiling, we compared ADM and adjacent PDAC tissues from patient samples to unveil the bridging genes, bridging signaling pathway and bridging molecular function during the malignant transformation of pancreatitis.

2022-07-25 | GSE208536 | GEO

Patient-derived organoids of pancreatic ductal adenocarcinoma for subtype determination and clinical outcome prediction

Project description:Two molecular subtypes of pancreatic ductal adenocarcinoma (PDAC) have been proposed: the “Classical” and “Basal-like” subtypes. However, the “molecular” classification has not been applied in real-world clinical practice. This study aimed to establish patient-derived organoids (PDOs) for PDAC and evaluate their application in subtype classification and clinical outcome prediction. We constructed a PDO library for morphologic and RNA-seq analyses and drug response assays in vitro. PDOs of PDAC were established at a high efficiency (> 70%) with at least 100,000 live cells. Morphologically, PDOs were classified as gland-like structures (GL type) or densely proliferating inside (DP type). RNA-seq analysis revealed that the “morphological” subtype (GL vs. DP) roughly corresponded to the “molecular” subtype (“Classical” vs. “Basal-like”). The proposed “morphological” classification predicted clinical treatment response and prognosis; the median overall survival of patients with GL type were significantly longer than that of those with DP type (P < 0.005). The GL type showed a better response to gemcitabine than the DP type in vitro, whereas the drug response of the DP type was improved by the combination of ERK and autophagy inhibition. PDAC PDOs facilitated subtype determination and clinical outcome prediction, thereby advancing precision medicine for PDAC.

2024-04-11 | GSE228801 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data