Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Pancreatic Cancer Cell Lines

PROVIDER: PRJNA944630 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25534135_1.fastq.gz	Fastqsanger.gz
	SRR25534135_2.fastq.gz	Fastqsanger.gz
	SRR25534136_1.fastq.gz	Fastqsanger.gz
	SRR25534136_2.fastq.gz	Fastqsanger.gz
	SRR25534137_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Homo sapiens

Project description:Pancreatic Cancer Cell Lines Sequencing

| PRJNA238816 | ENA

Transcriptome analysis of human pancreatic cancer cell lines and gemcitabine-resistant pancreatic cancer cell lines

Project description:Transcriptome analysis of human pancreatic cancer cell lines and gemcitabine-resistant pancreatic cancer cell lines

| PRJNA588180 | ENA

Homo sapiens

Project description:Pancreatic Cancer Cell Lines Transcriptome Sequencing

| PRJNA238817 | ENA

Unravelling altered RNA metabolism in pancreatic cancer cells by liquid-chromatography coupling to ion mobility mass spectrometry

Project description:Ion mobility coupling to mass spectrometry facilitates an increase of resolution and chromatographic peak-capacity. Further coupling to liquid chromatography results in multi-dimensional analytical methods, especially suitable for complex matrices with structurally similar compounds. Modified nucleosides are a large group of very similar members and are linked to aberrant proliferation. Contiguous to basal production under physiological conditions, they are increasingly excreted by transformed cells and subsequently discussed as putative biomarkers for various cancer types. Therefore, they are discussed as putative biomarkers for various cancer types. Here we report a method for modified nucleosides covering 37 species. We determined collisional cross-sections with high reproducibility from pure analytical standards. We applied an optimized phenyl-boronic acid solid-phase extraction on media obtained from four different pancreatic cancer cell lines. Our analysis could discriminate different sub-types of pancreatic cancer cell lines. Importantly, they clearly separated from a pancreatic control cell line and blank medium. m1A, m27G and Asm were the most important features discriminating cancer cell lines derived from well differentiated and poorly differentiated cancers. Eventually, we suggest the analytical method reported here for future tumor-marker identification studies.

2019-05-16 | MTBLS812 | MetaboLights

Profiling of Kallikrein Proteases and Global Proteome Biology of PDAC, Chronic Pancreatitis and Normal Pancreas

Project description:Cell conditioned medium from human pancreatic cancer cell lines MiaPaCa-2, AsPC-1, primary pancreatic cell lines as well as human FFPE tissue samples from pancreatic ductal adenocarcinoma (PDAC), chronic pancreatitis (CP), ampullary cancer, non-malignant adjacent pancreas and normal pancreas were analyzed via targeted (SRM, PRM) and/or explorative (DIA) mass spectrometry.

| MSV000090255 | MassIVE

Homo sapiens

Project description:Molecular subtypes in pancreatic adenocarcinoma [pancreatic cancer cell lines]

| PRJNA311744 | ENA

Methylated microRNAs in Pancreatic cancer cell lines

Project description:Methylated microRNAs in Pancreatic cancer cell lines

| PRJNA487775 | ENA

Homo sapiens

Project description:Expression data from pancreatic cancer cell lines

| PRJNA126617 | ENA

DIA proteomics analysis of RNF223 knockdown and control pancreatic cancer cell lines

Project description:The proteome profiles of RNF223 knockdown and control pancreatic cancer cell lines were compared employing data independent acquisition(DIA) technology

2021-09-10 | PXD028446 |

Altered patterns of hydroxymethylation regulate oncogenic pathways in pancreatic cancer

Project description:Transcriptional deregulation of oncogenic pathways is a hallmark of cancer, and can be due to epigenetic alterations. 5-hydroxymethylcytosine is a recently discovered epigenetic modification that has not been studied in pancreatic cancer. Genome-wide analysis of 5-hmC enriched loci was conducted in low-passage pancreatic cancer cell lines and primary patient-derived xenografts and revealed strikingly altered patterns in neoplastic tissues. Differentially hydroxymethylated regions preferentially affected regulatory regions of the genome, specifically overlapping with H3K4me1 enhancers. Gain of 5-hmC was correlated with upregulation of the cognate transcripts, including many oncogenic pathways implicated in pancreatic neoplasia. Specifically, BRD4 was overexpressed and acquired 5hmC at enhancer regions in majority of neoplastic samples. Functionally, acquisition of 5hmC at BRD4 promoter regulated increase in transcript expression. Furthermore, blockade of BRD4 inhibited pancreatic cancer growth in vivo. In summary, redistribution of 5-hmC and preferential enrichment at oncogenic enhancers is a novel regulatory mechanism in human cancer. Genome-wide analysis of 5-hmC enriched loci was conducted in low-passage pancreatic cancer cell lines and primary patient-derived xenografts

2016-08-06 | E-GEOD-71839 | biostudies-arrayexpress

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