Single cell mRNA sequencing on esophageal cells of human biopsies coming from subtotal esophagectomy
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE311820 | GEO | 2026/02/03
REPOSITORIES: GEO
Similar Datasets
Project description:In this study, we used RNA sequencing to characterize esophageal progenitors following activation of the hedgehog (HH) pathway in vivo. We observed two main fates following activation of the HH pathway in the squamous epithelium: one population is in an intermediate state between squamous and columnar epithelium, and another achieves a full columnar conversion. We compared these 2 populations to different FACS sorted epithelial cells from different tissues of the gastro-intestinal tract (adult esophagus, embryonic esophagus, transition epithelium from the stomach, corpus of the stomach and small intestine). Our results suggest a multistep process in which esophageal progenitors first turn on a transcriptomic program that resembles the one from embryonic esophagus, then, a subset of these dedifferentiated cells can turn on a columnar differentiation program that shares similarities with intestinal cells. Collectively, these data demonstrate that some esophageal cells can be reprogrammed to generate columnar cells in vivo.
2021-04-20 | GSE148874 | GEO
Project description:In this study, we uncovered through single cell RNA sequencing (scRNA-seq) of mouse esophagus epithelium a population of taste buds clustered in the cervical segment of the esophagus. We compared this taste bud population to their lingual counterpart. We concluded that these taste buds have the same cellular composition than the ones from the tongue. State-of-the-art transcriptional regulatory network analysis allowed the identification of specific transcription factors associated to the differentiation of immature progenitors into the three different taste bud cell types in the tongue and the esophagus.
2023-03-09 | GSE220065 | GEO
Project description:The involvment of bile acids such as deoxycholic acid (DCA) in gastro-esophageal reflux disease and subsequent Barrett’s metaplsia has been postulated. This study examines gene expression induced by exposure to DCA in esophageal cells and may be utilised in cross-comparisions with data derived from gene expression studies of Barrett’s esophagus and associated adenocarcinoma. Additionally this study may be used to assess divergence in response to bile acids by comparisons with similar study performed in SKGT4 barrett''s assocaited adenocarcinoma cell line.
2010-02-20 | GSE13378 | GEO
Project description:The involvment of bile acids such as deoxycholic acid (DCA) in gastro-esophageal reflux disease and subsequent Barrettâ??s metaplsia has been postulated. This study examines gene expression induced by exposure to DCA in esophageal cells and may be utilised in cross-comparisions with data derived from gene expression studies of Barrettâ??s esophagus and associated adenocarcinoma. Additionally this study may be used to assess divergence in response to bile acids by comparisons with similar study performed in SKGT4 barrett''s assocaited adenocarcinoma cell line. HET-1A cells were exposed to 300um DCA over 24 hours in duplicate experiments including matched timepoint controls
2010-02-28 | E-GEOD-13378 | biostudies-arrayexpress
Project description:In this study we used single cell mRNA sequencing to explore heterogeneity of the fate induced by hedgehog (HH) pathway activation in esophageal cells. We merged the data from the two samples and filtered the merged data to work only with cells expressing the SmoM2-YFP protein (2,413 cells). Using UMAP reduction, we observed 10 clusters with a resolution set at 0.3. Among these clusters, we identified clusters of squamous esophagus epithelial cells but also one cluster enriched for many columnar markers. These results show that activation of the HH pathway in esophageal keratinocytes leads to multiple cell phenotypes including a columnar epithelial one in a minority of keratinocytes.
2021-04-20 | GSE148875 | GEO
Project description:Esophageal adenocarcinoma arises from Barrett s esophagus, the precancerous metaplastic replacement of squamous by columnar epithelium in response to chronic inflammation. Development of adenocarcinoma is accompanied by non-genetic plasticity of epithelial and stromal cells. Multiomics profiling, integrating single-cell transcriptomics, extracellular matrix proteomics, tissue mechanics and spatial multiplexed proteomics of 64 samples from 12 patient trajectories of progression from normal epithelium, to metaplasia, dysplasia and adenocarcinoma, revealed shared and patient-specific progression paths. We detected profound consistent alterations of type and composition of tumor microenvironment cells, matrix composition and cell neighborhoods. Stromal cells with characteristics of cancer-associated fibroblasts appear early at the premalignant metaplastic stage. Thus, Barrett s esophagus progresses as a coordinated multi-component system, supporting a treatment paradigm that incorporates tissue reprogramming beyond targeting cancerous cells.
2023-02-25 | MSV000091366 | MassIVE
Project description:Barrett's esophagus is a metaplastic condition of the distal esophagus, characterized by the replacement of normal squamous epithelium by columnar epithelium. Patients with BE have an increased risk of developing esophageal adenocarcinoma. MicroRNAs have been implicated to be disease and tissue specific, however limited data of microRNA expression in the esophagus is available. Therefore we evaluated microRNA expression profiles of esophageal adenocarcinoma and compared these with Barrett's esophagus and normal squamous esophagus.
2012-03-15 | GSE29965 | GEO
Project description:<p>BEAGESS is a genome-wide association study (GWAS) which takes advantage of the extensive data collected by investigators in the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON, <a href="http://beacon.tlvnet.net/">http://beacon.tlvnet.net</a>), representing many of the high-quality population-based and other epidemiologic studies of BE and EA in the world. The overall goal of our research is to evaluate the influence of genetic susceptibility on risk of EA and its main precancerous condition, BE.</p> <p>The primary aims of the study are to identify tagSNPs most strongly associated with risk of esophageal adenocarcinoma (EA) and Barrett's esophagus (BE). In the secondary aims we will evaluate the extent to which the most significant associations vary according to key environmental and host factors for these conditions, including gender, obesity and cigarette smoking. These results will guide additional exploratory analyses examining ways in which individual SNP results might be aggregated to shed light in the importance of specific pathways relevant to the etiology of BE and EA, and to identify possible epistatic effects.</p>
| phs000869 | dbGaP
Project description:Barrett Esophagus (BE) is a risk factor for the development of esophageal adenocarcinoma (EAC). As endemic obesity emerges as a risk factor for increasing numbers of EAC we utilized our IL-1b mouse model of BE to understand the impact of a high fat diet (HFD) on disease progression. Indeed, increased dysplasia development in HFD treated IL-1b mice correlated with an accelerated cytokine response with specific upregulation of IL-8 in esophageal tissue, which could be confirmed by specific overexpression of IL-8 in the BE mouse model. Consequently we observed an influx of immature myeloid cells and neutrophils resulting in a decrease of regulatory NK T cells. HFD led to a specific shift in the gut microbiome, similar to that in human BE patients, being responsible for a specific inflammatory phenotype with elevated IL-1b and IL-8 which could be eliminated under germ free conditions and lead to an increased influx of cardia (Lgr5) stem cells into the esophagus giving rise to dysplasia.
2019-04-30 | GSE103616 | GEO
Project description:<p><b>Background:</b> Use of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has been shown to protect against tetraploidy, aneuploidy, and chromosomal alterations in the metaplastic condition Barrett's esophagus (BE) and to lower the incidence and mortality of esophageal adenocarcinoma (EA). The esophagus is exposed to both intrinsic and extrinsic mutagens resulting from gastric reflux, chronic inflammation and exposure to environmental carcinogens such as those found in cigarettes. Here we test the hypothesis that NSAID use inhibits accumulation of point mutations/indels during somatic genomic evolution in BE. <b>Methods:</b> Whole exome sequences were generated from 82 purified epithelial biopsies and paired blood samples from a cross-sectional study of 41 NSAID users and 41 nonusers matched by sex, age, smoking, and continuous time using or not using NSAIDs. <b>Results:</b> NSAID use reduced overall frequency of point mutations across the spectrum of mutation types, lowered the frequency of mutations even when adjusted for both <i>TP53</i> mutation and smoking status, and decreased the prevalence of clones with high variant allele frequency. Never smokers who consistently used NSAIDs had fewer point mutations in signature 17, which is commonly found in EA. NSAID users had on average a 50% reduction in functional gene mutations in nine cancer-associated pathways and also had less diversity in pathway mutational burden compared to nonusers. <b>Conclusions:</b> These results indicate NSAID use functions to limit overall mutations on which selection can act and supports a model in which specific mutant cell populations survive or expand better in the absence of NSAIDs. Galipeau PC, et al. Genome Med. 2018 Feb 27;10(1):17. PMID: <a href="https://www.ncbi.nlm.nih.gov/pubmed/29486792" target="_blank">29486792</a>.</p>
| phs001654 | dbGaP