Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA311748 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Molecular subtypes in pancreatic adenocarcinoma [pancreatic cancer cell lines]
| PRJNA311744 | ENA
Project description:MicroRNA Expression Patterns to Differentiate Pancreatic Adenocarcinoma From Normal Pancreas and Chronic Pancreatitis
2010-03-11 | E-TABM-664 | biostudies-arrayexpress
Project description:Molecular subtypes in pancreatic adenocarcinoma
| PRJNA311745 | ENA
Project description:Prognostic relevance of molecular subtypes and master regulators in pancreatic ductal adenocarcinoma
| PRJNA263337 | ENA
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
Project description:BACKGROUND & AIMS: Pancreatic ductal adenocarcinoma (PDAC) is usually incurable. Contrary to genetic mechanisms involved in PDAC pathogenesis, epigenetic alterations are ill defined. Here we determine the contribution of epigenetically silenced genes to the development of PDAC. METHODS: We investigated methylated DNAs from PDACs, chronic pancreatitis and normal pancreatic tissues using Methyl-CpG immunoprecipitation followed by microarray hybridization. Promoter methylation of selected genes was confirmed with the Epityper assay. Expression levels were evaluated by quantitative RT-PCR. WNK2 was further investigated in tissue microarrays, methylation analysis of early pancreatic intraepithelial neoplasia (PanINs), mouse models for PDAC and pancreatitis, re-expression studies after demethylation, and cell growth assays using WNK2 overexpression. RESULTS: A total of 3.8% of 27.800 interrogated CpG islands were hypermethylated in PDAC versus normal and chronic pancreatitis tissues. Hypermethylation was confirmed in 12 out of 13 selected islands and was associated with gene silencing in 4 of them. The most prominently hypermethylated gene, WNK2, was further investigated. Demethylation assays confirmed the link between methylation and expression. WNK2 hypermethylation was higher in pancreatic tumor cells than in surrounding inflamed tissues and was observed in PanIN lesions as well as in a PDAC mouse model. WNK2 mRNA and protein expression were lower in PDAC and chronic pancreatitis compared to normal tissues both in patients and mouse models. Overexpression of WNK2 led to a reduced cell growth and WNK2 expression in tissues correlated negatively with the expression of pERK1/2, a downstream target of WNK2 responsible for cell proliferation. CONCLUSIONS: WNK2 is downregulated by promoter hypermethylation early in PDAC pathogenesis and may support tumor cell growth via the ERK-MAPK pathway. 3 types of pancreatic tissue samples: 5 normals, 2 chronic pancreatitis, 7 tumors (PDAC)
2012-11-01 | E-GEOD-37480 | biostudies-arrayexpress
Project description:The goal of the study was to examine the transcriptional profile of pancreatic tumors to identify molecular subtypes in order to develop validated clinically useful gene expression signature with the potential to guide therapy decision. Tissue was obtained by snap freezing in liquid nitrogen as soon as removed. All tissue samples were stored at -80C. Samples were embedded in OCT and a 4ug section was taken for H/E staining. After QC procedure to ensure high quality RNA (RIN>7) and confirm PDAC histology, 78 samples were subjected to microarray analysis. All patients signed an Institutional Review Board approved consent for bio-banking, clinical data extraction and molecular analysis. 85 samples (77 tumors, 3 normal and 5 pancreatitis) were compared to a mixed reference pool of 66 tumor samples to identify gene expression patterns.
2016-06-01 | E-GEOD-77858 | biostudies-arrayexpress
Project description:Pancreatic ductal adenocarcinoma (PDAC) remains a lethal disease with a 5-year survival of 4%. A key hallmark of PDAC is extensive stromal involvement, which makes capturing precise tumor-specific molecular information difficult. Here, we have overcome this problem by applying blind source separation to a diverse collection of PDAC gene expression microarray data, which includes primary, metastatic, and normal samples. By digitally separating tumor, stroma, and normal gene expression, we have identified and validated two tumor-specific subtypes including a “basal-like†subtype which has worse outcome, and is molecularly similar to basal tumors in bladder and breast cancer. Furthermore, we define 'normal' and 'activated' stromal subtypes which are independently prognostic. Our results provide new insight into the molecular composition of PDAC which may be used to tailor therapies or provide decision support in a clinical setting where the choice and timing of therapies is critical. Analysis of the landscape of gene expression in pancreatic adenocarcinoma. Data include 145 primary and 61 metastatic PDAC tumors, 17 cell lines, 46 pancreas and 88 distant site adjacent normal samples. Arrays represent distinct samples. The SPOT column in the raw data file (linked to each sample record) contains Agilent feature extraction numbers (included in the 'GPL4133-20424.txt' linked to the platform records).
2015-09-07 | E-GEOD-71729 | biostudies-arrayexpress
Project description:Currently it is unknown whether activation of recruited or resident pancreatic fibroblasts, including pancreatic stellate cells activation, create a common “fibroblast-activated phenotype” indistinguishable from their associated-diseased microenvironment . Using a combination of microRNA and mRNA profiling of fibroblasts isolated from pancreatic ductal adenocarcinoma (PDAC), chronic pancreatitis (CP), periampullary cancer (PAT) and areas of histologically normal pancreas, followed by comprehensive validation, we show that activated fibroblasts derived from different pancreatic disease types are considerably distinct.
2020-07-14 | GSE123377 | GEO
Project description:Pancreatitis is triggered by environmental or cellular stress and is the leading contributor to pancreatic ductal adenocarcinoma. Altered gene expression in response to acinar cell stress determines the severity and duration of pancreatitis. However, it is unclear what factors contribute to this phenomenon. Here, we define a novel role for Activating Transcription Factor 3 (ATF3) during pancreatic injury. ATF3, a key mediator in the unfolded protein response, is robustly expressed in acinar cells during pancreatitis. Targeted deletion of Atf3 altered the molecular response to injury, with Atf3-/- acinar cells maintaining cell organization in response to cerulein, a well-established inducer of pancreatitis. Characterization of the mechanism using chromatin immunoprecipitation followed by Next Generation sequencing (ChIP-seq) identified 11,771 enrichment spots for ATF3, with known transcriptional start sites for >3,000 genes within 5 kb of ATF3 enrichment. Gene ontology analysis revealed a significant representation of ATF3 enrichment to genes affecting cell organization, including Mist1, a molecule required for establishing acinar cell organization. We confirmed a direct interaction of ATF3 to the Mist1 promoter during pancreatitis, and showed that ATF3 is required for altered Mist1 expression in response to injury. Finally, we demonstrate that ATF3 repression of Mist1 involves HDAC5. These findings suggest that ATF3 is a key transcriptional regulator during pancreatitis and promotes loss of the mature acinar cell phenotype in response to pancreatic injury. Two samples were produced from male mice 4 hours after CIP initiation from intraparitoneal injections of cerulein, a ChIP sample using an ATF3 antibody and an IP control.
2015-08-01 | E-GEOD-60250 | biostudies-arrayexpress