Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Increased PXR and suppressed T-cell signaling are associated with malignant degeneration of Barrett’s esophagus

ABSTRACT: Barrett’s esophagus (BE) is the precursor lesion for esophageal adenocarcinoma (EAC). To detect EAC in early stage, patients with BE undergo endoscopic surveillance. Surveillance cohorts largely consist of non-dysplastic Barrett’s esophagus (NDBE) patients with a low annual progression risk (<0.5%). Predictive biomarkers for malignant progression of NDBE could improve efficacy of surveillance. Biomarker research has mostly focused on aberrant protein expression on BE epithelial cells. Moreover, insight in cell signaling driving malignant transformation is unknown. This study uses a data-driven approach to analyze tumor-stroma interaction in NDBE which progressed to high grade dysplasia (HGD) or EAC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE210647 | GEO | 2023/01/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Alteration of protein expression and spliceosome pathway activity during Barrett’s carcinogenesis.

Project description:Esophageal adenocarcinoma (EAC) is a common and aggressive type of cancer and Barrett’s esophagus (BE) is a known precursor lesion and the strongest risk factor for EAC. Prediction of risk is currently based on histologic examination which is challenged by problems such as inter-observer variability due to high heterogeneity of the dysplastic tissue. Molecular markers might offer an additional way to understand carcinogenesis and improve diagnosis and eventually treatment. .

2021-09-09 | PXD020903 | Pride

Esophageal tissue and serum microRNAs changed in the progression of Barrett’s esophagus in mice

Project description:Circulating microRNAs (miRNAs) are promising biomarkers for the early detection of cancers. This assay aimed to address potential circulating miRNAs to monitor the progression from Barrett’s esophagus to esophageal adenocarcinoma (EAC).

2017-12-06 | GSE100390 | GEO

DCLK1 as a Marker/Indicator of Stem Cell Response in Barrett’s Esophagus/Esophageal Adenocarcinoma

Project description:The hypotheses are: 1) the intestinal stem cell marker, DCLK1, which is increased in both the epithelium and stroma in colon cancer is also increased in BE (Barrett’s esophagus) with HGD (high grade dysplasia) and in EAC (esophageal adenocarcinoma), 2) this expression correlates with disease progression towards EAC and 3) eradication of cells expressing stem cell markers occurs after therapy of EMR (endoscopic mucosal resection) or RFA (radiofrequency ablation) to eradicate BE with HGD and intramucosal adenocarcinoma and esophagectomy for EAC. We will test our hypotheses with the following aims: 1) To characterize the cell specific expression patterns of intestinal stem cell biomarkers in BE patients and correlate them with serum expression and disease progression, 2) To examine prospectively the effects of EMR, RFA or esophagectomy on the expression of stem cell biomarkers and the progression to EAC.

| 2273018 | ecrin-mdr-crc

Global DNA methylation patterns in Barrett’s esophagus, dysplastic Barrett’s, dysplastic Barrett’s, and esophageal adenocarcinoma are associated with BMI, gender, and tobacco use

Project description:Background: The risk of developing Barrett’s esophagus (BE) and/or esophageal adenocarcinoma (EAC) is associated with specific demographic and behavioral factors, including gender, obesity/elevated body-mass index (BMI), and tobacco use. Alterations in DNA methylation, an epigenetic modification that can affect gene expression and that can be influenced by environmental factors, is frequently present in both BE and EAC and is believed to play a role in the formation of BE and its progression to EAC. It is currently unknown whether obesity or tobacco smoking influence the risk of developing BE/EAC via the induction of alterations in DNA methylation. To investigate this possibility, we assessed the genome-wide methylation status of 81 esophageal tissues, including BE, dysplastic BE, and EAC epithelia using HumanMethylation450 BeadChips (Illumina). Results: We found numerous differentially methylated loci in the esophagus tissues when comparing males to females, obese to lean individuals, and smokers to nonsmokers. Differences in DNA methylation between these groups were seen in a variety of functional genomic regions, and both within and outside of CpG islands. Several cancer-related pathways were found to have differentially methylated genes between these comparison groups. Conclusions: Our findings suggest obesity and tobacco smoking may influence DNA methylation in the esophagus and raise the possibility that these risk factors affect the development of BE, dysplastic BE, and EAC through influencing the epigenetic status of specific loci that have a biologically plausible role in cancer formation.

2016-10-25 | GSE89181 | GEO

Bile acids promote adenocarcinoma in a novel transgenic mouse model of Barrett’s esophagus

Project description:Esophageal adenocarcinoma (EAC) has the fastest increase of any cancer in the US and Europe, and arises in the setting of Barrett’s esophagus (BE), defined by replacement of normal squamous epithelium with columnar intestinal-like epithelium. BE is thought to result from chronic esophageal inflammation but has been elusive to model in animals. Herein, we have generated the first transgenic mouse model of Barrett’s esophagus through overexpression of interleukin-1ß (IL-1β). IL-1β overexpression in the mouse esophageal mucosa induces chronic inflammation that progresses to intestinal metaplasia, with characteristic expression of TFF2, Bmp4 and Cdx2. With aging, IL-1b transgenic mice progress to esophageal adenocarcinoma (EAC) but the process is markedly accelerated by exposure to bile acids and/or nitrosamines, resembling the human counterpart. Moreover, progenitor cells present in the gastric cardia, but absent from the esophagus in humans and mice, are increased in BE, suggesting the cell of origin in the gastric cardia

2011-01-31 | GSE24931 | GEO

MicroRNA expression signatures in Barrett's esophagus and esophageal adenocarcinoma

Project description:Esophageal adenocarcinoma (EAC) is a highly aggressive malignancy that frequently develops from Barrett’s esophagus (BE), a premalignant pathological change occurring in the lower end of esophagus. To identify BE patients at high risk of malignant transformation is essential to the prevention of EAC. Although microRNA (miRNA) expression signatures have been associated with the etiology and prognosis of several types of cancers, their roles in the development of EAC have not been extensively evaluated.

2009-12-31 | GSE16456 | GEO

Global Phospho-Proteomic Profiling of Pathway-Level Molecular Alterations in Barrett’s Esophagus

Project description:In the present study, we applied deep, quantitative mass-spectrometry to clinical samples (Barrett’s esophagus and matched adjacent normal biopsies) to gain a mechanistic understanding of the molecular pathways associated with disease progression. From our rich LC/MS profiles, we identified a robust proteomic signature that was able to correctly classify independent samples on disease status. Projection of this same signature against EAC tumor profiles was strongly predictive of survival outcomes, while subsequent comparative analysis with published BE transcriptomic profiles provided independent evidence in support of these results. Further, our phosphoproteomic analysis revealed signaling pathways specifically and significantly altered in BE relative to paired controls, providing some mechanistic insights into the cellular dysregulation of key components of specific processes that likely drives disease progression.

2022-08-11 | PXD023293 | Pride

HOXA13 in etiology and oncogenic potential of Barrett’s esophagus [EPC2]

Project description:Barrett’s esophagus in gastrointestinal reflux patients constitutes a columnar epithelium with distal characteristics, prone to progress to esophageal adenocarcinoma. HOX genes are known mediators of position-dependent morphology. Here we show HOX collinearity in the adult gut while Barrett’s esophagus shows high HOXA13 expression in stem cells and their progeny. HOXA13 overexpression appears sufficient to explain both the phenotype (through downregulation of the epidermal differentiation complex) and the oncogenic potential of Barrett’s esophagus. Intriguingly, employing a mouse model that contains a reporter coupled to the HOXA13 promotor we identify single HOXA13-positive cells distally from the physiological esophagus, which is mirrored in human physiology, but increased in BE. Additionally, we observe that HOXA13 expression confers a competitive advantage to cells. We thus propose that Barrett’s esophagus and associated esophageal adenocarcinoma is the consequence of expansion of this gastro-esophageal HOXA13-expressing compartment following epithelial injury.

2021-04-24 | GSE173169 | GEO

HOXA13 in etiology and oncogenic potential of Barrett’s esophagus [BAR-T]

2021-04-24 | GSE173166 | GEO

HOXA13 in etiology and oncogenic potential of Barrett’s esophagus [KH2 mESC diff]

2021-04-24 | GSE173168 | GEO