ReviewProgress in molecular biology and translational science2010
Oxyntic atrophy, metaplasia, and gastric cancer.
Review in Progress in molecular biology and translational science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 64 citations in OpenAlex.
- The hyaluronic acid receptor CD44 coordinates normal and metaplastic gastric epithelial progenitor cell proliferation.The Journal of biological chemistry · 2013Trial
- Cell plasticity in cancer and therapy resistance.Experimental & molecular medicine · 2026Review
- PSMD14-mediated PFKFB2 deubiquitination activates H3K27 lactylation to drive cancer stemness in gastric adenocarcinoma.Cell death and differentiation · 2026Article
- Review
- Pyroptosis in gastric mucosal injury‑related diseases (Review).International journal of molecular medicine · 2025Review
- Emerging role of spasmolytic polypeptide-expressing metaplasia in gastric cancer.Journal of gastrointestinal oncology · 2024Review
- TRIF-IFN-I pathway iniScience · 2024Article
- Role and research progress of spasmolytic polypeptide‑expressing metaplasia in gastric cancer (Review).International journal of oncology · 2024Article
- Histopathological features of glandular atrophy of the lamina propria of the gastric mucosa during its occurrence and development.BMC gastroenterology · 2023Article
- Role of spasmolytic polypeptide-expressing metaplasia in gastric mucosal diseases.American journal of cancer research · 2023Review
- Molecular pathogenesis, targeted therapies, and future perspectives for gastric cancer.Seminars in cancer biology · 2022Review
- Inflammation and Gastric Cancer.Diseases (Basel, Switzerland) · 2022Review
- SLC26A9 deficiency causes gastric intraepithelial neoplasia in mice and aggressive gastric cancer in humans.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Gastric epithelial histology and precancerous conditions.World journal of gastrointestinal oncology · 2022Review
- Regulation of the double-stranded RNA response through ADAR1 licenses metaplastic reprogramming in gastric epithelium.JCI insight · 2022Article
- A Bibliometric Analysis of Atrophic Gastritis From 2011 to 2021.Frontiers in medicine · 2022Article
- A tumour-resident Lgr5Nature cell biology · 2021Article
- Iqgap3-Ras axis drives stem cell proliferation in the stomach corpus during homoeostasis and repair.Gut · 2021Article
- Molecular Landscapes of Gastric Pre-Neoplastic and Pre-Invasive Lesions.International journal of molecular sciences · 2021Review
- WFDC2 Promotes Spasmolytic Polypeptide-Expressing Metaplasia Through the Up-Regulation of IL33 in Response to Injury.Gastroenterology · 2021Article
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
Gastric carcinogenesis involves the loss of parietal cells (oxyntic atrophy) and subsequent replacement of the normal gastric lineages with metaplastic cells. In humans, two metaplastic lineages develop as sequelae of chronic Helicobacter pylori infection: intestinal metaplasia and spasmolytic polypeptide-expressing metaplasia (SPEM). Mouse models of both chronic Helicobacter infection and acute pharmacological oxyntic atrophy have led to the discovery that SPEM arises from transdifferentiation of mature chief cells. The presence of inflammation promotes the expansion of SPEM in mice. Furthermore, studies in Mongolian gerbils as well as increasing evidence from human studies indicate that SPEM likely represents a precursor for the development of intestinal metaplasia. These findings suggest that loss of parietal cells, augmented by chronic inflammation, leads to a cascade of metaplastic events. Identification of specific biomarkers for SPEM and intestinal metaplasia hold promise for providing both early detection of preneoplasia and information on prognostic outcome following curative resection.
Indexed as
Identifiers
What OpenQuestion holds
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.