Profiling upper gastrointestinal microbiota in esophageal disease
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB48716 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR9552690_1.fastq.gz | Fastqsanger.gz | |||
| ERR9552690_2.fastq.gz | Fastqsanger.gz | |||
| ERR9552700_1.fastq.gz | Fastqsanger.gz | |||
| ERR9552700_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 873 |
Similar Datasets
Project description:To test the hypothesis that there is a specific miRNA expression signature which characterizes Barrett's esophagus development and progression, we performed miRNA microarray analysis comparing normal esophageal squamous epithelium with the two different metaplastic lesions occuring within Barrett's mucosa (i.e. gastric metaplasia and intestinal metaplasia). Samples of H. pylori-related gastritis and gastric intestinal metaplasia were also considered in the definition of esophageal-specific miRNAs.
2011-01-01 | GSE24839 | GEO
Project description:To test the hypothesis that there is a specific miRNA expression signature which characterizes Barrett's esophagus development and progression, we performed miRNA microarray analysis comparing normal esophageal squamous epithelium with the two different metaplastic lesions occuring within Barrett's mucosa (i.e. gastric metaplasia and intestinal metaplasia). Samples of H. pylori-related gastritis and gastric intestinal metaplasia were also considered in the definition of esophageal-specific miRNAs. miRNA microarray analysis was performed in a series of samples obtained from (a) 10 histologically-proven long-segment Barrett's esophagus patients; (b) 10 patients with H. pylori-related chronic atrophic gastritis. Overall, 10 normal esophageal squamous epithelium samples, 10 esophageal intestinal metaplasia samples, 10 esophageal gastric metaplasia samples, 10 H. pylori -related gastritis samples (no atrophic lesion detected; obtained from the antrum) and 10 gastric intestinal metaplasia samples (obtained from the antrum) were considered.
2011-01-01 | E-GEOD-24839 | biostudies-arrayexpress
Project description:The goal of this experiment is to characterize the copy number changes in esophageal mucosa of patients with Barrett's esophagus (BE) who progress to esophageal dysplasia and adenocarcinoma (BE progressors), as compared to patients with BE who do not progress for at least two years after esophageal mucosal sampling (non-progressors with never dysplastic Barrett's esophagus - NvDBE - samples). We sampled esophageal mucosa from the following groups: 1) non-dysplastic intestinal metaplasia from 16 patients at least 1 year before progression to esophageal dysplasia or adenocarcinoma (PP-BE); 2) non-dysplastic intestinal metaplasia from 21 patients who did not progress to dysplasia or adenocarcinoma for at least 2 years of surveillance after the tested sample (NvDBE) 3) non-dysplastic intestinal metaplasia from 21 patients who had temporally concurrent but spatially separate intestinal metaplasia samples from the same procedure (C-BE). 4) 10 samples of esophageal dysplasia or adenocarcinoma from patients in group 1 and 3. Samples were obtained by endoscopic biopsy, endomucosal resection or surgical resection, processed for clinical purposes by routine histopathologic methods, including formalin fixation and paraffin embedding (FFPE). DNA was extracted from 5 micro tissue sections of FFPE blocks and DNA extracted using QIAamp DNA FFPE Tissue Kit (Qiagen, Germantown, MD). Samples were processed for identification of somatic copy number alterations using the OncoScan FFPE Assay or the OncoScan CNV Assay (Affymetrix, Santa Clara, CA) according to the manufacturer's protocols. After hybridization, the arrays were washed, stained using GeneChip Fluidics Station 450 (Affymetrix) and scanned using GeneChip Scanner 3000 7G (Affymetrix). The CEL files generated are deposited here.
2019-10-27 | E-MTAB-7396 | biostudies-arrayexpress
Project description:The role of acid and bile salts in the pathogenesis of esophageal carcinoma arising from Barrett's metaplasia has been well established. Cell proliferation of Barrett's epithelium in response to pulsatile acid exposure has since been confirmed in vivo using endoscopy specimens. Histone deactylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis to assess the ability of HDAC-42 to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Experiment Overall Design: SEG-1 cells were pretreated for 24 hours with vehicle or HDAC-42, pulsed with media or acidified media (pH 3.5; 20 mins at 37C), replenished with media or HDAC-42, and harvested 6 hours later. Global gene expression analysis was conducted using the human genome chip U133 2.0 Plus.
2008-06-15 | E-GEOD-7964 | biostudies-arrayexpress
Project description:The role of acid and bile salts in the pathogenesis of esophageal carcinoma arising from Barrett's metaplasia has been well established. Cell proliferation of Barrett's epithelium in response to pulsatile acid exposure has since been confirmed in vivo using endoscopy specimens. Histone deactylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis to assess the ability of HDAC-42 to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Keywords: acid-pulsed cells pretreated with HDAC inhibitor or vehicle
2007-07-30 | GSE7964 | GEO
Project description:The aim of this study is to generate and validate biomarkers to stratify patients with Barrett’s esophagus in terms of risk for developing cancer. We studied gene expression profiling in 69 frozen specimens, consisting of esophageal squamous epithelium from 19 healthy subjects, 20 specimens from patients with Barrett’s esophagus and 21 cases of esophageal adenocarcinoma, 9 cased of esophageal squamous cell carcinoma by whole genome microarray analysis. Laser capture microdissection technique was applied to procure cells from defined regions of Barrett’s esophagus metaplasia and esophageal adenocarcinoma. Microarray results were validated by quantitative real-time polymerase chain reaction (qRT-PCR) in an independent cohort consisting of 42 cases. Furthermore, immunohistochemistry was performed using antibodies to two selected target molecules on a third independent cohort of 36 specimens, consisting of 36 cases. A total of 1176 genes were associated significantly with esophageal adenocarcinoma. The expression pattern of a 4 gene signature with the highest discriminant score based on linear discriminant analysis (GeneSpring GX10.2), was identified and validated by qRT-PCR in independent cohort.
2013-10-18 | GSE26886 | GEO
Project description:Title: In vitro and in vivo effects of the orally bioavailable phenylbutyrate-derived histone deacetylase inhibitor OSU-HDAC42 on gene expression in esophageal tissues and in esophageal adenocarcinoma cells; Histone deacetylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis at multiple time-points to assess the ability of OSU-HDAC42, the S enantiomer of the previously published compound HDAC-42, to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Experiment Overall Design: SEG-1 cells were pretreated for 24 hours with vehicle or OSU-HDAC42, pulsed with acidified media (pH 3.5; 20 mins at 37C), replenished with media or OSU-HDAC42, and harvested 3, 6 and 24 hours later. Global gene expression analysis was conducted using the human genome chip U133 2.0 Plus.
2008-04-05 | E-GEOD-9974 | biostudies-arrayexpress
Project description:The aim of this study is to generate and validate biomarkers to stratify patients with Barrett’s esophagus in terms of risk for developing cancer. We studied gene expression profiling in 69 frozen specimens, consisting of esophageal squamous epithelium from 19 healthy subjects, 20 specimens from patients with Barrett’s esophagus and 21 cases of esophageal adenocarcinoma, 9 cased of esophageal squamous cell carcinoma by whole genome microarray analysis. Laser capture microdissection technique was applied to procure cells from defined regions of Barrett’s esophagus metaplasia and esophageal adenocarcinoma. Microarray results were validated by quantitative real-time polymerase chain reaction (qRT-PCR) in an independent cohort consisting of 42 cases. Furthermore, immunohistochemistry was performed using antibodies to two selected target molecules on a third independent cohort of 36 specimens, consisting of 36 cases. A total of 1176 genes were associated significantly with esophageal adenocarcinoma. The expression pattern of a 4 gene signature with the highest discriminant score based on linear discriminant analysis (GeneSpring GX10.2), was identified and validated by qRT-PCR in independent cohort. Gene expression profiling of 20 specimens of Barrett's esophagus patients, 21 specimens of adenocarcinoma patients and 19 biopsies from patients with normal esophageal squamous epithelium, 9 specimens of squamous cell carcinoma were studied.
2011-10-31 | E-GEOD-26886 | biostudies-arrayexpress
Project description:Multi-omics of the esophageal microenvironment in reflux and metaplasia
| PRJEB46795 | ENA
Project description:Title: In vitro and in vivo effects of the orally bioavailable phenylbutyrate-derived histone deacetylase inhibitor OSU-HDAC42 on gene expression in esophageal tissues and in esophageal adenocarcinoma cells Histone deacetylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis at multiple time-points to assess the ability of OSU-HDAC42, the S enantiomer of the previously published compound HDAC-42, to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Keywords: acid-pulsed cells pretreated with OSU-HDAC42 or vehicle
2008-03-20 | GSE9974 | GEO