Observational studyGastroenterology2020
Notch Signaling Mediates Differentiation in Barrett's Esophagus and Promotes Progression to Adenocarcinoma.
Observational study in Gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed, 97 citations in OpenAlex.
- Randomized Controlled Trial of the Gastrin/CCKCancer prevention research (Philadelphia, Pa.) · 2021Trial
- Targeting the Notch signaling pathway in digestive system cancers: from bench to bedside.Cancer cell international · 2026Review
- Single-cell and bulk omics uncover fibroblast heterogeneity and HSPH1 as a key driver in Barrett's esophagus to esophageal adenocarcinoma progression.Cancer cell international · 2026Article
- Comparison of Invasive Interventions for Halting the Progression of Barrett's Esophagus.Cureus · 2026Review
- Paligenosis: dual potential of mature cell plasticity in regeneration and tumorigenesis.MedScience · 2026Review
- Targeting notch signaling pathway in esophageal cancer: from molecular insights to therapies.Oncology reviews · 2026Review
- Increased reflux secondary bile acids are associated with changes to the microbiome and transcriptome in Barrett's esophagus.Gut microbes · 2025Article
- The Interplay Between Esophageal Adenocarcinoma and Its Tumor Microenvironment: Toward Innovative Therapies.Cells · 2025Review
- LncRNA small nucleolar RNA host gene 1 (SNHG1) mediates acidic bile salt-induced EMT via the ULK1-Notch1 axis in Barrett's esophagus.Molecular biomedicine · 2025Article
- Probing Field Cancerization in the Gastrointestinal Tract Using a Hybrid Raman and Partial Wave Spectroscopy Microscope.Analytical chemistry · 2025Article
- Genetically Defined Organoid Models Reveal Mechanisms Driving Squamous Cell Neoplastic Evolution and Identify Potential Therapeutic Vulnerabilities.bioRxiv : the preprint server for biology · 2025Article
- Article
- The role of IL-33/ST2 axis in esophageal inflammatory diseases and cancers: implications for the immunopathogenesis and immunotherapeutic target?Therapeutic advances in gastroenterology · 2025Review
- Biomedical applications of organoids derived from the digestive system.Frontiers in cell and developmental biology · 2025Review
- Development of a ferroptosis-related signature and identification of NOTCH2 as a novel prognostic biomarker in pancreatic cancer.Frontiers in immunology · 2025Article
- Lysyl Oxidase Mediates Proliferation and Differentiation in the Esophageal Epithelium.Biomolecules · 2024Article
- Exosomal circular RNAs in tumor microenvironment: An emphasis on signaling pathways and clinical opportunities.MedComm · 2024Review
- Hybrid Raman and Partial Wave Spectroscopy Microscope for the Characterization of Molecular and Structural Alterations in Tissue.Journal of biophotonics · 2024Article
- Pathways regulating intestinal stem cells and potential therapeutic targets for radiation enteropathy.Molecular biomedicine · 2024Review
- Highlighting immune features of the tumor ecosystem and prognostic value of Tfh and Th17 cell infiltration in head and neck squamous cell carcinoma by single-cell RNA-seq.Cancer immunology, immunotherapy : CII · 2024Article
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Authors and funding
32 authors at 7 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsStudies are needed to determine the mechanism by which Barrett's esophagus (BE) progresses to esophageal adenocarcinoma (EAC). Notch signaling maintains stem cells in the gastrointestinal tract and is dysregulated during carcinogenesis. We explored the relationship between Notch signaling and goblet cell maturation, a feature of BE, during EAC pathogenesis.
methodsWe measured goblet cell density and levels of Notch messenger RNAs in BE tissues from 164 patients, with and without dysplasia or EAC, enrolled in a multicenter study. We analyzed the effects of conditional expression of an activated form of NOTCH2 (pL2.Lgr5.N2IC), conditional deletion of NOTCH2 (pL2.Lgr5.N2fl/fl), or loss of nuclear factor κB (NF-κB) (pL2.Lgr5.p65fl/fl), in Lgr5
resultsProgression of BE to EAC was associated with a significant reduction in goblet cell density comparing nondysplastic regions of tissues from patients; there was an inverse correlation between goblet cell density and levels of NOTCH3 and JAG2 messenger RNA. In mice, expression of the activated intracellular form of NOTCH2 in Lgr5
conclusionsNotch signaling contributes to activation of NF-κB and regulates differentiation of gastric cardia progenitor cells in a mouse model of BE. In human esophageal tissues, progression of BE to EAC was associated with reduced goblet cell density and increased levels of Notch expression. Strategies to block this pathway might be developed to prevent EAC in patients with BE.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.