ReviewCurrent opinion in gastroenterology2019
The cyclical hit model: how paligenosis might establish the mutational landscape in Barrett's esophagus and esophageal adenocarcinoma.
Review in Current opinion in gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
19 citing papers in PubMed, 27 citations in OpenAlex.
- Gastric hypoplasia in mice lacking fibroblast growth factor 9.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Article
- The preclinical discovery and development of zolbetuximab for the treatment of gastric cancer.Expert opinion on drug discovery · 2024Review
- Origins of cancer: ain't it just mature cells misbehaving?The EMBO journal · 2024Review
- The role of the fibroblast in Barrett's esophagus and esophageal adenocarcinoma.Current opinion in gastroenterology · 2024Review
- Molecular Pathology of Gastroesophageal Cancer.Clinics in laboratory medicine · 2024Review
- Success rate of current human-derived gastric cancer organoids establishment and influencing factors: A systematic review and meta-analysis.World journal of gastrointestinal oncology · 2024Article
- Gastric intestinal metaplasia: progress and remaining challenges.Journal of gastroenterology · 2024Review
- Shared features of metaplasia and the development of adenocarcinoma in the stomach and esophagus.Frontiers in cell and developmental biology · 2023Article
- Molecular pathogenesis, targeted therapies, and future perspectives for gastric cancer.Seminars in cancer biology · 2022Review
- An Endoscopic and Histologic Study on Healing of Radiofrequency Ablation Wounds in Patients With Barrett's Esophagus.The American journal of gastroenterology · 2022Article
- Paligenosis: Cellular Remodeling During Tissue Repair.Annual review of physiology · 2022Review
- Gastric Organoids: Progress and Remaining Challenges.Cellular and molecular gastroenterology and hepatology · 2022Review
- ELAPOR1 is a secretory granule maturation-promoting factor that is lost during paligenosis.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- ATF3 induces RAB7 to govern autodegradation in paligenosis, a conserved cell plasticity program.EMBO reports · 2021Article
- Molecular Pathology of Gastroesophageal Cancer.Surgical pathology clinics · 2021Review
- Profiles of autophagy-related genes in esophageal adenocarcinoma.BMC cancer · 2020Article
- Tumor organoids to study gastroesophageal cancer: a primer.Journal of molecular cell biology · 2020Review
- Metaplastic Paneth Cells in Extra-Intestinal Mucosal Niche Indicate a Link to Microbiome and Inflammation.Frontiers in physiology · 2020Review
- Roles for Autophagy in Esophageal Carcinogenesis: Implications for Improving Patient Outcomes.Cancers · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purpose of reviewIn this review, we explore a paligenosis-based model to explain Barrett's esophagus development and progression: 'the cyclical hit model.' RECENT
findingsGenomic analyses have highlighted the high mutational burden of esophageal adenocarcinoma, Barrett's esophagus, and even normal esophageal epithelium. Somatic mutations in key genes including TP53 occur early in the neoplastic progression sequence of Barrett's esophagus, whereas chromosomal amplification resulting in oncogene activation occurs as a critical late event. Paligenosis is a shared injury response mechanism characterized by activation of autophagy, expression of progenitor markers, and increased mTORC signaling-induced cell-cycle reentry. In the setting of chronic injury/inflammation, cycles of paligenosis may allow accumulation of mutations until eventually the mutational burden, in concert perhaps with mutations in key driver oncogenes, finally alters the cell's ability to redifferentiate, leading to the emergence of a potential neoplastic clone. SUMMARY: Under conditions of chronic gastroesophageal refluxate exposure, the normal esophageal squamous epithelium might undergo multiple cycles of paligenosis, allowing initially silent mutations to accumulate until key events impart mutant clones with an oncogenic survival advantage.
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Registered trials
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.