ArticleGut2025
Hybrid identity and distinct methylation profiles of incomplete intestinal metaplasia in the stomach.
Article in Gut, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- 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
- The "Hit-and-Run" legacy: epigenetic locking and the survival switch in H. pylori-associated gastric cancer.Cell death discovery · 2026Review
- Basal gland localization and focal distribution of OLFM4-expressing cells in increasing severity of gastric intestinal metaplasia.bioRxiv : the preprint server for biology · 2026Article
- Organoids for disease modeling and treatment: state-of-the-art.Experimental hematology & oncology · 2026Review
- Modeling the pre-metastatic niche of gastric cancer peritoneal metastasis under spatiotemporal resolution and investigating EVs-mediated immune suppression.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundGastric intestinal metaplasia (GIM), particularly the incomplete subtype (Inc IM), is strongly associated with increased gastric cancer (GC) risk. However, its role as a true precursor lesion remains uncertain.
objectiveWe aimed to delineate the molecular identity, differentiation potential and oncogenic relevance of Inc IM.
methodsSpatial transcriptomics using a custom lineage-enriched panel was applied to profile GIM and GC tissues. Subtype-specific GIM organoid models were developed for DNA methylation and chromatin accessibility profiling. Single-cell RNA sequencing was performed to evaluate differentiation capacity.
resultsSpatial transcriptomics revealed that Inc IM potentially originates from the deep antral gland cells and harbours a hybrid transcriptomic signature incorporating gastric, small intestinal and large intestinal lineages across both differentiated and stem/progenitor compartments. DNA methylation profiling of subtype-specific organoids showed that Inc IM exhibits extensive intergenic hypermethylation, resembling native antral mucosa. In contrast, complete subtype was marked by promoter hypermethylation of tumour suppressor genes and displayed a more fully intestinalised epigenetic profile. Organoid models recapitulated subtype-specific traits and demonstrated lineage plasticity. Spatial mapping of GC samples revealed an enrichment of Inc IM-like cells, particularly within microsatellite stable tumours. Approximately 76% of the GCs analysed were linked to GIM, while the remaining (24%) appeared to be associated with deep antral differentiation.
conclusionsInc IM represents a phenotypically unstable and epigenetically deregulated metaplastic state with dual-lineage potential and molecular resemblance to GC. These findings establish Inc IM as a true precursor to GC and underscore the importance of active surveillance and early intervention strategies.
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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.