{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"omics_type":["Metabolomics","Unknown","Transcriptomics","Genomics","Proteomics"],"submitter":["Syed Murtuza Baker"],"instrument_platform":["NextSeq 500"],"study_type":["scATAC-seq"],"organism":["Homo sapiens"],"species":["Homo sapiens"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-14128"],"description":["In the precursor pathology for oesophageal adenocarcinoma, Barrett’s oesophagus (BO), the adult stratified squamous epithelium is replaced by a simple columnar phenotype. This has been considered metaplasia; the inappropriate conversion from one adult cell-type to another. In fact, BO could be a reversal of mammalian embryogenesis when the early foregut is first lined by simple columnar epithelium. Exploring this hypothesis has been hampered by inadequate molecular details of human oesophageal development. Here, we adopted single cell transcriptomic and epigenomic approaches to discover and decode the cell types that constitute the initial primitive columnar, transitory and subsequently stratified lower oesophageal epithelium. Each stage is comprised of several previously undefined epithelial sub-populations. HNF4A, a major driver of the Barrett’s phenotype, is a prominent transcriptional regulator in the early foregut columnar cells, but not in the later ciliated or stratified cells, and is central to gene regulatory programmes known to be reactivated in BO. Moreover, GWAS susceptibility SNPs for BO mapped to putative regulatory regions in fetal epithelial cells, which are inaccessible in the corresponding adult epithelial cells. Collectively, these data argue that the path to BO involves de-differentiation to a primitive fetal-like state."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Nucleic Acid Extraction - Used 10X sample collection protocol, detailed in CG000505_chromium nuclei isolation kit_UG_RevA.pdf","Library Construction - Used 10X sample collection protocol, detailed in CG000505_chromium nuclei isolation kit_UG_RevA.pdf","Sample Collection - Human embryonic material was collected under ethical approval from the North West Research Ethics Committee (18/NW/0096), informed consent from all participants and according to the Codes of Practice of the Human Tissue Authority15. Tissue collection took place on our co-located clinical academic campus overseen by our research team ensuring immediate transfer to the laboratory. Embryonic material was staged by the Carnegie classification. Fetal material (after 56 dpc) was staged by foot length and ultrasound assessment. Individual tissues and organs were immediately dissected (Supplementary Data). In brief, describe the dissection. All visible adherent mesenchyme was removed under a dissecting microscope.","Sequencing - Used Illumina NextSeq 500 protocol, detailed in nextseq-500-system-guide-15046563-06.pdf"],"figure_sub":["Organization","MINSEQE Score","Assays and Data","MAGE-TAB Files"],"pubmed_authors":["Syed Murtuza Baker","Andrew Sharrocks"],"additional_accession":[]},"is_claimable":false,"name":"The Barrett’s precursor state to oesophageal adenocarcinoma shares features with transient cell populations in the developing human oesophagus - snATAC-seq","description":"In the precursor pathology for oesophageal adenocarcinoma, Barrett’s oesophagus (BO), the adult stratified squamous epithelium is replaced by a simple columnar phenotype. This has been considered metaplasia; the inappropriate conversion from one adult cell-type to another. In fact, BO could be a reversal of mammalian embryogenesis when the early foregut is first lined by simple columnar epithelium. Exploring this hypothesis has been hampered by inadequate molecular details of human oesophageal development. Here, we adopted single cell transcriptomic and epigenomic approaches to discover and decode the cell types that constitute the initial primitive columnar, transitory and subsequently stratified lower oesophageal epithelium. Each stage is comprised of several previously undefined epithelial sub-populations. HNF4A, a major driver of the Barrett’s phenotype, is a prominent transcriptional regulator in the early foregut columnar cells, but not in the later ciliated or stratified cells, and is central to gene regulatory programmes known to be reactivated in BO. Moreover, GWAS susceptibility SNPs for BO mapped to putative regulatory regions in fetal epithelial cells, which are inaccessible in the corresponding adult epithelial cells. Collectively, these data argue that the path to BO involves de-differentiation to a primitive fetal-like state.","dates":{"release":"2025-10-24T00:00:00Z","modification":"2025-10-24T16:43:47.941Z","creation":"2024-05-30T17:57:38.885Z"},"accession":"E-MTAB-14128","cross_references":{"ENA":["ERP160750"],"EFO":["EFO_0002944","EFO_0004170","EFO_0010891","EFO_0005518","EFO_0004184"]}}