Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA280121 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1950480.fastq.gz | Fastqsanger.gz | |||
| SRR1950490.fastq.gz | Fastqsanger.gz | |||
| SRR1950481.fastq.gz | Fastqsanger.gz | |||
| SRR1950482.fastq.gz | Fastqsanger.gz | |||
| SRR1950483.fastq.gz | Fastqsanger.gz |
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Project description:This SuperSeries is composed of the following subset Series: GSE40097: DNA methylation analysis of pancreatic cancer and non-malignant pancreas cell lines GSE40098: RNA expression analysis of pancreatic cancer and non-malignant pancreas cell lines GSE41794: DNA copy number profiling of 20 pancreatic cancer cell lines Refer to individual Series
2012-11-01 | E-GEOD-40099 | biostudies-arrayexpress
Project description:DNA methylation is an epigenetic mark associated with regulation of transcription and genome structure. These markers have been investigated in a variety of cancer settings for their utility in differentiating normal tissue from tumor tissue. Here, we examine the direct correlation between DNA methylation and patient survival. We find that changes in the DNA methylation of key pancreatic developmental genes is strongly associated with patient survival.
2015-04-02 | GSE67205 | GEO
Project description:Epigenetic modifications, particularly DNA methylation have been increasingly implicated in cancer. Although some genes display aberrant methylation in pancreatic cancer, a comprehensive global analysis is yet to be performed. To define the genome-wide pattern of DNA methylation in pancreatic ductal adenocarcinomas (PDAC), the methylation profile of 156 PDAC and 23 non-malignant pancreas was captured using high-density arrays. More than 90,000 CpG sites were significantly differentially methylated (DM) in PDAC relative to non-malignant pancreas, with pronounced alterations in a sub-set of 13,517 CpG sites. This sub-set of differentially methylated CpG sites segregated PDAC from non-malignant pancreas, regardless of tumour cellularity. As expected, PDAC hyper-methylation was most prevalent in the 5’ region of genes (including the proximal promoter, 5’UTR and CpG islands). From 3981 genes aberrantly methylated, approximately 36% showed significant correlation between methylation and mRNA expression levels. Pathway analysis revealed an enrichment of aberrant methylation in genes involved in key molecular mechanisms important to PDAC: TGF-β, WNT, Integrin signaling, Cell adhesion, Stellate cell activation and Axon guidance. Bisulfite amplicon deep sequencing and qRT-PCR expression analyses of axon guidance pathway genes SLIT2, SLIT3, ROBO1, ROBO3, SRGAP1, and MET suggested epigenetic suppression of SLIT-ROBO signaling and up-regulation of MET expression. Hypo-methylation of MET and ITGA2 correlated with high gene expression, which correlated with poor survival of PDAC patients. These data suggest that aberrant methylation plays an important role in pancreatic carcinogenesis affecting known core signaling pathways with important implications for disease pathophysiology and therapy. This dataset includes gene expression data from 103 primary tumour samples. 86 samples from this dataset have already been deposited into GEO (GSE36924), and has been duplicated here since the data has been processed differently. This data is also available through the International Cancer Genome Consortium (ICGC) Data Portal (http://dcc/icgc.org), under the project code: Pancreatic Cancer (QCMG, AU). Access to the restricted clinical data must be made through the ICGC Data Access Compliance Office (http://www.icgc.org/daco). This dataset contains gene expression array data from 103 primary pancreatic ductal adenocarcinoma samples. All samples have 1 biological replicate. These data have corresponding methylation 450K array data (GSE49149).
2014-05-05 | E-GEOD-50827 | biostudies-arrayexpress
Project description:Epigenetic processes such as DNA methylation play a key role in regulating tissue-specific and temporally-appropriate patterns of gene expression during development. Our knowledge about temporal changes to the epigenome in the developing human pancreas is limited. In this study we quantified levels of DNA methylation at over 800,000 sites in 112 human fetal pancreatic samples (51 male and 61 female) spanning from 6 to 21 post conception weeks (pcw). We found dramatic changes in DNA methylation across human pancreas development, with >22% of all methylation sites displaying significant changes across developmental age, with the majority of these sites showing stable levels of DNA methylation in the mature pancreas. Sites associated with developmental changes in DNA methylation during fetal pancreas development were significantly underrepresented in promoter regulatory regions but significantly overrepresented in regions flanking CpG islands (shores and shelves) and gene bodies. Highly significant differences in DNA methylation were observed between males and females at a number of autosomal sites, with a small number of regions showing sex-specific DNA methylation trajectories across pancreas development. Weighted gene correlation network analysis (WGCNA) revealed modules of co-methylated loci associated with developmental age were enriched for genes involved in maturity onset diabetes of the young (MODY) and other metabolic phenotypes. A comparison with developmentally-dynamic patterns of DNA methylation in the developing human brain revealed significant tissue specific differences between the fetal pancreas and the fetal brain. Our data confirms the prenatal period to be a time of dynamic epigenetic changes. To our knowledge, this is the most extensive study of DNA methylation patterns in human fetal pancreatic development.
2024-02-19 | GSE244636 | GEO
Project description:The purpose of this study is to establish a registry of patients with pancreatic diseases. Patients included in the registry may include those with: pancreatic cancer, precancerous lesions of the pancreas, inflammatory lesions of the pancreas, cystic lesions of the pancreas, and patients at high-risk of pancreatic cancer such as those with a family history of pancreatic cancer or with a family history of a syndrome known to be associated with pancreatic cancer. Pancreatic cancer is the fourth leading cause of death from cancer in the United States. However, little is known about the development of pancreatic cancer and pancreatic diseases in individuals with the above conditions. Knowledge of how family history, environmental exposures, and inflammatory lesion of the pancreas contribute to the development of pancreatic cancer and pancreatic diseases is essential.
You may qualify to take part in this research study because you have inflammation in the pancreas, a pancreatic cyst, pre-cancerous lesions of the pancreas, pancreatic cancer, a family history of pancreatic cancer, or a family history of a syndrome known to be associated with pancreatic cancer.
We will also be collecting a blood sample from all participants for DNA isolation. Sometimes we are born with genes or DNA that give us an increased or decreased chance of developing an illness later in life. Genetic material will be isolated from your blood for further study. You may also choose to provide additional blood samples for serum and plasma extraction. Serum and plasma are components of the blood which can be used to measure indicators of disease in the blood, called biomarkers,for pancreatic diseases. Clinical data and biological specimens contained in this study may be used for a wide variety of future related studies to the cause, diagnosis, outcome and treatment of pancreatic cancer.
Funds for conducting this research are provided by Mount Sinai.
| 2215393 | ecrin-mdr-crc
Project description:This is a mathematical model of pancreatic cancer that includes descriptions of pancreatic cancer cells, pancreatic stellate cells, effector cells and tumor-promoting and tumor-suppressing cytokines to investigate the effects of immunotherapies on patient survival.
2024-09-02 | BIOMD0000000792 | BioModels
Project description:The pancreas is a special organ which is considered both endocrine and exocrine. The exocrine pancreas gives rise to pancreatic ductal adenocarcinoma (PDAC), which accounts for the majority of pancreatic cancer cases. In recent years, various new therapeutic options for cancer patients have resulted in increased survival, but these advancements do not include PDAC patients, who still present with a 5-year survival rate of only 13%. Therefore, there is an increasing need for finding new therapeutic targets to treat PDAC. Here, we identify the chromatin binding protein HMGB2 as a promising option. HMGB2 is overexpressed in multiple cancer types and correlates with their replicative potential. Using multiple models from patient tissue to organoids and mice, we assign a key role to HMGB2 in the proliferation control of PDAC. Using single-cell multiomics, we uncover how HMGB2 affects chromatin accessibility at a plethora of cell cycle-related gene loci, thereby directly controlling their expression. We further demonstrate how HMGB2 pharmacological targeting constrains cell proliferation and accordingly propose that it represents a ubiquitous and attractive anti-proliferative target in the fight against PDAC.
2026-06-04 | GSE296809 | GEO
Project description:The pancreas is a special organ which is considered both endocrine and exocrine. The exocrine pancreas gives rise to pancreatic ductal adenocarcinoma (PDAC), which accounts for the majority of pancreatic cancer cases. In recent years, various new therapeutic options for cancer patients have resulted in increased survival, but these advancements do not include PDAC patients, who still present with a 5-year survival rate of only 13%. Therefore, there is an increasing need for finding new therapeutic targets to treat PDAC. Here, we identify the chromatin binding protein HMGB2 as a promising option. HMGB2 is overexpressed in multiple cancer types and correlates with their replicative potential. Using multiple models from patient tissue to organoids and mice, we assign a key role to HMGB2 in the proliferation control of PDAC. Using single-cell multiomics, we uncover how HMGB2 affects chromatin accessibility at a plethora of cell cycle-related gene loci, thereby directly controlling their expression. We further demonstrate how HMGB2 pharmacological targeting constrains cell proliferation and accordingly propose that it represents a ubiquitous and attractive anti-proliferative target in the fight against PDAC.
2026-06-04 | GSE296808 | GEO
Project description:The pancreas is a special organ which is considered both endocrine and exocrine. The exocrine pancreas gives rise to pancreatic ductal adenocarcinoma (PDAC), which accounts for the majority of pancreatic cancer cases. In recent years, various new therapeutic options for cancer patients have resulted in increased survival, but these advancements do not include PDAC patients, who still present with a 5-year survival rate of only 13%. Therefore, there is an increasing need for finding new therapeutic targets to treat PDAC. Here, we identify the chromatin binding protein HMGB2 as a promising option. HMGB2 is overexpressed in multiple cancer types and correlates with their replicative potential. Using multiple models from patient tissue to organoids and mice, we assign a key role to HMGB2 in the proliferation control of PDAC. Using single-cell multiomics, we uncover how HMGB2 affects chromatin accessibility at a plethora of cell cycle-related gene loci, thereby directly controlling their expression. We further demonstrate how HMGB2 pharmacological targeting constrains cell proliferation and accordingly propose that it represents a ubiquitous and attractive anti-proliferative target in the fight against PDAC.
2026-06-04 | GSE296819 | GEO
Project description:The pancreas is a special organ which is considered both endocrine and exocrine. The exocrine pancreas gives rise to pancreatic ductal adenocarcinoma (PDAC), which accounts for the majority of pancreatic cancer cases. In recent years, various new therapeutic options for cancer patients have resulted in increased survival, but these advancements do not include PDAC patients, who still present with a 5-year survival rate of only 13%. Therefore, there is an increasing need for finding new therapeutic targets to treat PDAC. Here, we identify the chromatin binding protein HMGB2 as a promising option. HMGB2 is overexpressed in multiple cancer types and correlates with their replicative potential. Using multiple models from patient tissue to organoids and mice, we assign a key role to HMGB2 in the proliferation control of PDAC. Using single-cell multiomics, we uncover how HMGB2 affects chromatin accessibility at a plethora of cell cycle-related gene loci, thereby directly controlling their expression. We further demonstrate how HMGB2 pharmacological targeting constrains cell proliferation and accordingly propose that it represents a ubiquitous and attractive anti-proliferative target in the fight against PDAC.
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