ArticleGastroenterology2010
Mature chief cells are cryptic progenitors for metaplasia in the stomach.
Article in Gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 205 papers.
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Who cites it
205 citing papers in PubMed, 272 citations in OpenAlex.
- The hyaluronic acid receptor CD44 coordinates normal and metaplastic gastric epithelial progenitor cell proliferation.The Journal of biological chemistry · 2013Trial
- Distribution of LGR5+ cells and associated implications during the early stage of gastric tumorigenesis.PloS one · 2013Trial
- Review
- The origins and progression of pyloric metaplasia following gastric mucosal injury.Physiological reviews · 2026Review
- Reframing early gastric carcinogenesis through lineage, niche, and evolution.Cancer metastasis reviews · 2026Review
- Diet-Induced Obesity ExacerbatesbioRxiv : the preprint server for biology · 2026Article
- Gastric intestinal metaplasia: unraveling the multifactorial pathogenesis and advancing risk stratification for gastric cancer prevention.Cellular and molecular life sciences : CMLS · 2026Review
- Helicobacter pylori-induced PPFIA4 orchestrates immune network-promoting gastritis and gastric bacterial colonization.The Journal of clinical investigation · 2026Article
- Regulation of STK38 by autophagy governs YAP1 activity during paligenosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Animal models and pathogenesis of gastric cancer: from premalignant conditions-to-metastasis.Cancer biology & medicine · 2026Review
- Multimerin1 and not Galectin-8 tempers WNT signaling to promote gastric chief cell differentiation.Scientific reports · 2026Article
- Mechanistic insights into the evolution from spasmolytic polypeptide-expressing metaplasia to gastric cancer (Review).Molecular biology reports · 2026Review
- Recent advances in spasmolytic polypeptide expressing metaplasia research.World journal of gastrointestinal oncology · 2026Review
- Roles of interleukins in spasmolytic polypeptide‑expressing metaplasia (Review).International journal of oncology · 2026Review
- The mechanical niche in gastric precancer: extracellular matrix remodeling, mechanotransduction, and stem-cell fate.Frontiers in cell and developmental biology · 2026Review
- Regulation and Function of Sox2 and CD44 Expression in the Stomach by Bone Morphogenetic Protein Signaling.Gastro hep advances · 2026Article
- Epithelial WNT secretion drives niche escape of developing gastric cancer.Molecular cancer · 2025Article
- Reprogramming the Course of Precancer with Targeted Therapeutic Intervention: Lessons from Interception in Gastric Preneoplasia.Cancer prevention research (Philadelphia, Pa.) · 2025Review
- Review
- Multimerin1, not Galectin-8, Promotes Gastric Chief Cell Differentiation by Tempering WNT Signaling.bioRxiv : the preprint server for biology · 2025Article
145 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsGastric cancer evolves in the setting of a pathologic mucosal milieu characterized by both loss of acid-secreting parietal cells and mucous cell metaplasias. Indeed, mucous cell metaplasia is considered the critical preneoplastic lesion for gastric cancer. Previous investigations have shown that infection of mice with Helicobacter felis or induction of acute parietal cell loss with the drug DMP-777 leads to the emergence of a type of metaplasia designated spasmolytic polypeptide-expressing metaplasia (SPEM). We have hypothesized that SPEM arises from proliferating cells in gland bases, either from a cryptic progenitor cell or by transdifferentiation of mature chief cells.
methodsTaking advantage of the chief cell-restricted expression of Mist1-Cre-ER(T2), we used lineage mapping to examine whether SPEM lineages were derived from chief cells in 3 independent models of induction by DMP-777 treatment, L-635 treatment, or H felis infection.
resultsTreatment of mice with L-635 for 3 days led to rapid parietal cell loss, induction of a prominent inflammatory infiltrate, and emergence of SPEM. In all 3 models, SPEM developed, at least in part, from transdifferentiation of chief cells. We further found that acute parietal cell loss in the setting of inflammation (L-635 treatment) led to more rapid induction and expansion of SPEM derived from transdifferentiation of chief cells.
conclusionsThese studies provide direct evidence by lineage tracing that SPEM evolves from differentiated chief cells. Thus, mature gastric chief cells have the ability to act as cryptic progenitors and reacquire proliferative capacity within the context of mucosal injury and inflammation.
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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.