Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA146489 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Dysplasia and early cancer are hard to detect in endoscopic biopsies and hence this study was carried out to evaluate the biomarker potential of DNA methylation to detect dyspasia and early cancer in Barrett's esophaghus patients. Bisulfite converted genomic DNA was hybridized onto Illumina 27k methylation arrays. 22 Barrett's esophagus (BE) and 2 Duodenum vs. 24 esophageal adenocarcinoma (EAC)
2013-01-28 | E-GEOD-32925 | biostudies-arrayexpress
Project description:Dysplasia and early cancer are hard to detect in endoscopic biopsies and hence this study was carried out to evaluate the biomarker potential of DNA methylation to detect dyspasia and early cancer in Barrett's esophaghus patients. Bisulfite converted genomic DNA was hybridized onto Illumina 27k methylation arrays.
2013-01-28 | GSE32925 | GEO
Project description:RNA-seq was performed on esophageal adenocarcinoma (EAC), Barrett's without dysplasia, Barrett's with low-grade dysplasia (LGD) and normal squamous esophagus tissue to find early alterations in the transcriptome level turning Barrett's dysplastic.
2017-07-23 | E-MTAB-4054 | biostudies-arrayexpress
Project description:We pursued the hypothesis that epigenetic regulators of transcription are involved in both the development and the progression of HPV-associated CIN. Using HELP-tagging, we performed the most comprehensive study to date of DNA methylation in HPV-associated cervical neoplasia, testing ~2 million loci throughout the human genome in biopsies from 78 HPV+ women, identifying changes starting in early CIN and maintained through carcinogenesis. We identified loci at which DNA methylation is consistently altered, beginning early in the course of neoplastic disease and progressing with disease advancement. DNA methylation profiles for cervical biopsies of 19 normals, 20 CIN1, 16 CIN2/3, and 23 cervical cancers.
2016-08-22 | E-GEOD-76986 | biostudies-arrayexpress
Project description:We pursued the hypothesis that epigenetic regulators of transcription are involved in both the development and the progression of HPV-associated CIN. Using HELP-tagging, we performed the most comprehensive study to date of DNA methylation in HPV-associated cervical neoplasia, testing ~2 million loci throughout the human genome in biopsies from 78 HPV+ women, identifying changes starting in early CIN and maintained through carcinogenesis. We identified loci at which DNA methylation is consistently altered, beginning early in the course of neoplastic disease and progressing with disease advancement.
2016-08-22 | GSE76986 | 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 all the phenotypic lesions seen in the Barrett's carcinogenic process miRNA microarray analysis was performed in a series of 14 normal esophageal squamous epithelium samples, 14 Barrett's mucosa samples, 7 low-grade intra-epithelial neoplasia samples, 5 high-grade intra-epithelial neoplasia samples and 11 Barrett's adenocarcinoma samples
2010-01-29 | E-GEOD-20099 | biostudies-arrayexpress
Project description:We took saliva samples from 89 people with oesophageal cancer (plus 9 with high grade dysplasia, also labelled here as cancer) and 167 controls. We took replicate samples on 6 cancer samples and 4 controls to assess reproducibility. The cancer groups comprise people with invasive adenocarcinoma (61 and also 6 replicates), 28 people with intramucosal adenocarcinoma, 9 people with high-grade dysplasia arising in Barrett's esophagus, 52 patients with non-dysplastic Barrett's esophagus, 42 people with no positive diagnosis after endoscopy (ie no Barrett's, + 1 replicate), and 73 self-reported healthy volunteers (with 3 duplicates)
2024-02-07 | GSE232332 | GEO
Project description:In humans with UC, low-grade dysplasia also develops predominantly in the distal colon, progresses more rapidly to neoplasia than proximal colon low-grade dysplasia and associates with worse patient prognosis. In a mouse model of colitis-associated carcinogenesis induced by administration of the mutagen AOM and the luminal toxin DSS, tumors also develop exclusively in the distal part of the large intestine. We monitored global changes in the transcriptome of mouse proximal and distal colon during exposure to AOM/DSS with the aim to define biological pathways and processes that characterize regional responses of the large intestine to colitis-associated carcinogenesis.
2015-06-01 | GSE64658 | GEO
Project description:This study was conducted to explore the serum methylome of precancerous lesions belonging to the serrated pathway of colorectal carcinogenesis in a prospective multicentre cohort. Individuals were grouped into five main categories: (i) serrated adenocarcinoma (SAC), (ii) high-risk serrated polyps (HR-SP) comprising traditional serrated adenomas (TSA), sessile serrated lesions (SSL), and serrated polyps (SP) with dysplasia or ≥ 10 mm; (iii) high-risk hyperplastic polyps (HR-HP), defined as HP ≥ 10 mm; (iv) low-risk serrated lesions (LR-SL) including SP without dysplasia < 10 mm and HP < 10 mm; and (v) healthy individuals with no colorectal findings (NCF). First, epigenome-wide methylation levels were quantified in pooled cfDNA samples to characterize the differential methylation profile between no serrated neoplasia (NSN: NCF and LR-SL) and high-risk serrated lesions (HR-SL: HR-HP and HR-SP); concordance with tissue methylation levels was assessed using external datasets. Then, the pathway-specific cfDNA methylation signature was evaluated together with cfDNA pools from the conventional CRC pathway. cfDNA was extracted from serum samples and methylation measurements were assessed with the Infinium MethylationEPIC BeadChip. Data was mainly preprocessed and analyzed with R/Bioconductor packages.
2024-03-01 | GSE199173 | GEO
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