Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA860071 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR20307600_1.fastq.gz	Fastqsanger.gz
	SRR20307600_2.fastq.gz	Fastqsanger.gz
	SRR20307501_1.fastq.gz	Fastqsanger.gz
	SRR20307501_2.fastq.gz	Fastqsanger.gz
	SRR20307601_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 384

Similar Datasets

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

PHARMACOLOGICAL INHIBITION AND REVERSAL OF PANCREATIC ACINAR DUCTAL METAPLASIA

Project description:Acinar ductal metaplasia (ADM), is believed to be one of the earliest precursor lesions towards the development of pancreatic ductal adenocarcinoma, and maintaining the pancreatic acinar cell phenotype suppresses tumor formation. We report that pStat3 and HDAC inhibition can attenuate ADM in vitro and TSA treatment reverses the dedifferentiated phenotype to one that is more acinar. Our findings suggest that pharmacological inhibition or reversal of pancreatic ADM represents a potential therapeutic strategy for blocking ductal reprogramming of acinar cells.

2022-07-01 | GSE195560 | GEO

Transcriptional Profile Of Human Pancreatic Acinar Ductal Metaplasia

Project description:Aberrant acinar to ductal metaplasia (ADM), one of the earliest events involved in exocrine pancreatic cancer development, is typically studied using pancreata from transgenic mouse models. We used primary, human pancreatic acinar cells to evaluate the transcriptional profile during the course of ADM.

2022-06-01 | GSE179248 | GEO

ST6Gal1 sialyltransferase promotes acinar to ductal metaplasia and pancreatic cancer progression

Project description:This study describes a novel function for the ST6GAL1 sialyltransferase in promoting acinar to ductal metaplasia (ADM). ST6GAL1 activity facilitates ADM by reprogramming acinar cells into a more progenitor-like state.

2023-09-05 | GSE234045 | GEO

Transcriptional Profile Of Human Pancreatic Acinar Ductal Metaplasia

Project description:Transcriptional Profile Of Human Pancreatic Acinar Ductal Metaplasia

| PRJNA742923 | ENA

PHARMACOLOGICAL INHIBITION AND REVERSAL OF PANCREATIC ACINAR DUCTAL METAPLASIA

Project description:PHARMACOLOGICAL INHIBITION AND REVERSAL OF PANCREATIC ACINAR DUCTAL METAPLASIA

| PRJNA801251 | ENA

ST6Gal1 sialyltransferase promotes pancreatic ductal adenocarcinoma by facilitating acinar to ductal metaplasia

Project description:ST6Gal1 sialyltransferase promotes pancreatic ductal adenocarcinoma by facilitating acinar to ductal metaplasia

| PRJNA716991 | ENA

Epigenetic Small Molecule Library Screen for Inhibition and Reversal of Acinar to Ductal Metaplasia in a Mouse Pancreas 3-Dimensional Organoid Model

Project description:We used in vitro mouse pancreatic 3-D organoid model to screen for possible compounds that inhibit or reverse Acinar-to-Ductal Metaplasia, which is a known intial stage of pancreatic ductal adenocarcinoma (PDAC). This model has higher translational value due to the harbored KRASG12D mutation which is common in PDAC patients and is considered a driving mutatrion for cancer development. Observed transcriptomic differences with select hit compounds compared to vehicle control could be very useful for future targeted therapy approach, as well as for further understanding of the driving mechanisms involved in pancreatic metaplasia and PDAC. Some of the hit compounds are already FDA approved drugs that could be easily re-purposed for PDAC treatment or prevention.

2024-01-26 | GSE236292 | GEO

FRA1 controls acinar cell plasticity during murine KrasG12D-induced pancreatic acinar to ductal metaplasia

Project description:FRA1 controls acinar cell plasticity during murine KrasG12D-induced pancreatic acinar to ductal metaplasia

| PRJNA986430 | ENA

mTORC1 and mTORC2 converge on the Arp2/3 complex to promote KrasG12D-induced acinar-to-ductal metaplasia and early pancreatic carcinogenesis

Project description:Oncogenic KrasG12D, a driver mutation of pancreatic ductal adenocarcinoma (PDAC), induces neoplastic transformation of acinar cells through acinar-to-ductal metaplasia (ADM). Here, we show that both functional complexes of mTOR (mechanistic target of rapamycin kinase, mTORC1 and mTORC2) are specifically activated in ADM. Murine models uncover that mTORC1 and mTORC2 cooperate to promote KrasG12D-driven ADM development. Proteomic analyses identify Arp2/3 complex, an actin nucleator, as the common downstream effector: mTORC1 is responsible for the protein synthesis of Rac1 and Arp3 while mTORC2 promotes the Arp2/3 complex activity via Akt/Rac1 signalling. Genetic ablation of Arp2/3 complex completely arrests KrasG12D-driven ADM development. The Arp2/3 complex-mediated y-branching of actin network promotes the basolateral spread of filamentous actin, which is indispensable for acinar cells-initiated carcinogenesis. Induced by oncogenic KrasG12D, ADM is a metaplastic phenotype of acinar cells that requires extensive actin rearrangements. mTORC1 and mTORC2, downstream targets of KrasG12D, have well-established oncogenic functions in PDAC development. The actin-related protein 2/3 (Arp2/3) complex is the first identified actin nucleator. Regarded as textbook knowledge, it is activated by EGFR/Rac1 signalling to promote the polymerisation of branched actin filaments from pre-existing filaments in numerous biological contexts. Hereby, we identify that mTORC1 and mTORC2 attain a dual, yet non-redundant, regulatory role in promoting Arp2/3 complex function, which is responsible for generating basolateral filamentous actin in ADM. Thus, the role of Arp2/3 complex fills up the missing gap between putative oncogenic signals and actin dynamics underlying PDAC initiation.

2021-01-07 | PXD018296 | Pride

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