ArticleGut2020
DNA damage signalling as an anti-cancer barrier in gastric intestinal metaplasia.
Article in Gut, 2020. 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
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
19 citing papers in PubMed, 21 citations in OpenAlex.
- Reframing early gastric carcinogenesis through lineage, niche, and evolution.Cancer metastasis reviews · 2026Review
- Stromal BMP signalling maintains stem cell genome integrity and prevents gastric cancer initiation.Cell death & disease · 2026Article
- Gastric Epithelium from BRCA1 and BRCA2 Carriers Harbors Increased Double-Stranded DNA Damage and Enhanced Growth Potential.Molecular cancer research : MCR · 2026Article
- Gastric intestinal metaplasia: unraveling the multifactorial pathogenesis and advancing risk stratification for gastric cancer prevention.Cellular and molecular life sciences : CMLS · 2026Review
- Interaction between ELMO1 DNA methylation and Med31 promotes H. pylori-induced gastric cancer EMT and intestinal metaplasia via M2 polarization.Scientific reports · 2026Article
- Pan-Cancer Analysis of WRN: From Multi-Omics Biomarker Discovery to Therapy-Guiding Functional Evidence.OncoTargets and therapy · 2026Article
- The mechanical niche in gastric precancer: extracellular matrix remodeling, mechanotransduction, and stem-cell fate.Frontiers in cell and developmental biology · 2026Review
- Gastric epithelium frombioRxiv : the preprint server for biology · 2025Article
- Helicobacter pylori, microbiota and gastric cancer - principles of microorganism-driven carcinogenesis.Nature reviews. Gastroenterology & hepatology · 2025Review
- Modeling gastric intestinal metaplasia in 3D organoids using nitrosoguanidine.Journal of molecular cell biology · 2024Article
- A Natural Peptide from A Traditional Chinese Medicine Has the Potential to Treat Chronic Atrophic Gastritis by Activating Gastric Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Gastric intestinal metaplasia: progress and remaining challenges.Journal of gastroenterology · 2024Review
- Article
- Article
- Article
- H2AFX might be a prognostic biomarker for hepatocellular carcinoma.Cancer reports (Hoboken, N.J.) · 2023Article
- Alterations in bacterial community dynamics from noncancerous to Gastric cancer.Frontiers in microbiology · 2023Article
- Article
- Ferroptosis Patterns Correlate with Immune Microenvironment Characterization in Gastric Cancer.International journal of general medicine · 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
18 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIntestinal metaplasia (IM) is a premalignant stage that poses a greater risk for subsequent gastric cancer (GC). However, factors regulating IM to GC progression remain unclear. Previously, activated DNA damage response (DDR) signalling factors were shown to engage tumour-suppressive networks in premalignant lesions. Here, we interrogate the relationship of DDR signalling to mutational accumulation in IM lesions.
designIM biopsies were procured from the gastric cancer epidemiology programme, an endoscopic surveillance programme where biopsies have been subjected to (epi)genomic characterisation. IM samples were classified as genome-stable or genome-unstable based on their mutational burden/somatic copy-number alteration (CNA) profiles. Samples were probed for DDR signalling and cell proliferation, using the markers γH2AX and MCM2, respectively. The expression of the gastric stem cell marker, CD44v9, was also assessed. Tissue microarrays representing the GC progression spectrum were included.
resultsMCM2-positivity increased during GC progression, while γH2AX-positivity showed modest increase from normal to gastritis and IM stages, with further increase in GC. γH2AX levels correlated with the extent of chronic inflammation. Interestingly, genome-stable IM lesions had higher γH2AX levels underscoring a protective anti-cancer role for DDR signalling. In contrast, genome-unstable IM lesions with higher mutational burden/CNAs had lower γH2AX levels, elevated CD44v9 expression and modest promoter hypermethylation of DNA repair genes
conclusionsOur data suggest that IM lesions with active DDR will likely experience a longer latency at the premalignant state until additional hits that override DDR signalling clonally expand and promote progression. These observations provide insights on the factors governing IM progression.
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.