Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Intratumor transcriptome changes in PDAC

PROVIDER: PRJNA1042652 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26875018_1.fastq.gz	Fastqsanger.gz
	SRR26875018_2.fastq.gz	Fastqsanger.gz
	SRR26875019_1.fastq.gz	Fastqsanger.gz
	SRR26875019_2.fastq.gz	Fastqsanger.gz
	SRR26875020_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Transcriptome profiling of glioblastoma biopsies obtained by neuro-navigation in four distinct areas for 10 patients (necrotic zone, tumor zone, interface, and peripheral brain zone).

Project description:We classified samples and deciphered a key genes signature of intratumor heterogeneity by Principal Component Analysis and Weighted Gene Co-expression Network Analysis. Transcriptome analysis highlighted a pronounced intratumor architecture reflecting the surgical sampling plan of the study and identified gene modules associated with hallmarks of cancer.

2016-09-19 | E-MTAB-5092 | biostudies-arrayexpress

Mapping functional to morphological variation reveals the basis of regional extracellular matrix subversion and nerve invasion in pancreatic cancer [RNA-seq]

Project description:Intratumor morphological heterogeneity of pancreatic ductal adenocarcinoma (PDAC) predicts clinical outcomes but is only partially understood at the molecular level. To elucidate the gene expression programs underpinning intratumor morphological variation in PDAC, we investigated and deconvoluted at single cell level the molecular profiles of histologically distinct clusters of PDAC cells. We identified three major morphological and functional variants that co-exist in varying proportions in all PDACs, display limited genetic diversity, and are associated with a distinct organization of the extracellular matrix: a glandular variant with classical ductal features; a transitional variant displaying abortive ductal structures and mixed endodermal and myofibroblast-like gene expression; and a poorly differentiated variant lacking ductal features and basement membrane, and showing neuronal lineage priming. Ex vivo and in vitro evidence supports the occurrence of dynamic transitions among these variants in part influenced by extracellular matrix composition and stiffness and associated with local, specifically neural, invasion.

2024-03-25 | GSE208732 | GEO

Mapping functional to morphological variation reveals the basis of regional extracellular matrix subversion and nerve invasion in pancreatic cancer [DNA-seq]

2024-03-25 | GSE209951 | GEO

Mapping functional to morphological variation reveals the basis of regional extracellular matrix subversion and nerve invasion in pancreatic cancer [RNA-Seq3]

2024-03-25 | GSE243584 | GEO

Mapping functional to morphological variation reveals the basis of regional extracellular matrix subversion and nerve invasion in pancreatic cancer [RNA-Seq2]

2024-03-25 | GSE243583 | GEO

MYC ecDNA promotes intratumour heterogeneity and plasticity in PDAC

Project description:Intratumor heterogeneity and phenotypic plasticity drive tumour progression and therapy resistance. Oncogene dosage variation contributes to cell state transitions and phenotypic heterogeneity, thereby providing a substrate for somatic evolution. Nonetheless, the genetic mechanisms underlying phenotypic heterogeneity are still poorly understood. Here, we show that extrachromosomal DNA (ecDNA) is a major source of high-level focal amplification in key oncogenes and a major contributor of MYC heterogeneity in pancreatic ductal adenocarcinoma (PDAC). We demonstrate that ecDNAs drive varying levels of MYC dosage, depending on their regulatory landscape, enabling cancer cells to rapidly and reversibly adapt to microenvironmental changes. In absence of selective pressure, a high ecDNA copy number imposes a substantial fitness cost on PDAC cells. We also show that MYC dosage affects cell morphology and dependence of cancer cells on stromal niche factors. Our work provides the first detailed analysis of ecDNAs in PDAC and describes a new genetic mechanism driving MYC heterogeneity in PDAC.

2024-12-29 | GSE281325 | GEO

MYC ecDNA promotes intratumour heterogeneity and plasticity in PDAC

2024-12-29 | GSE247129 | GEO

Exocrine and connective tissue signatures in early pancreatic adenocarcinoma foci and their surrounding tissue

Project description:This project is reporting on microdissection proteomics of human operable, non-neoadjuvant treated pancreatic ductal adenocarcinomas (PDAC) with deep coverage of histologically neoplastic and adjacent healthier exocrine glands as well as stromal regions surrounding both. Through proteomic analysis, the parenchymal sample types differed significantly, with the malignant regions characterized by a broad downregulation of digestive enzymes. Instead, the stromal areas were alike, dominated by extracellular matrix proteins and lower expression of most metabolic pathways compared to the exocrine areas. Cholesterol synthesizing enzymes were more abundant in the tumor than stroma, as confirmed by an independent PDAC dataset and immunohistochemistry of PDAC microarrays. However, this was not accompanied by intratumor lipid deposition. Pathways most prognostic for survival were unexpectedly enriched in the histologically healthier exocrine glands, with a specific prognostic marker. Systematic analysis of pancreatic cancer transcriptomes from The Cancer Genome Atlas revealed that increased transcriptional complexity confers poor prognosis in PDAC.

2022-09-05 | PXD026371 | Pride

Project description:Intratumor microbiota changes in pancreatic cancer

| PRJNA1041943 | ENA

RNA-sea of Smad4 wild-type or Smad4 knockout KvPC PDAC organoids from monocultures or co-cultures with pancreatic stellate cells and RNA-seq of flow-sorted PSCs from the same co-cultures.

Project description:RNA-sequencing of flow-sorted Smad4 wild-type (WT) or Smad4 knockout (KO) KvPC (i.e. KRASG12V; p53 mutant) pancreatic ductal adenocarcinoma (PDAC) organoids from monocultures or co-cultures with pancreatic stellate cells (PSCs) and RNA-sequencing of flow-sorted PSCs from the same co-cultures. We investigated changes in transcriptome in Smad4 KO KvPC PDAC organoids compared to Smad4 WT KvPC PDAC organoids in monoculture or in co-culture with PSCs. We also investigated the changes in transcriptome in PSCs co-cultured with Smad4 WT or Smad4 KO KvPC PDAC organoids.

2024-12-02 | GSE263081 | 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