# Stratified management of residual gastric cancer risk after Helicobacter pylori eradication

**Authors:** Li Song, Qi-Ying Yu

PMC · DOI: 10.3389/fmicb.2026.1779490 · Frontiers in Microbiology · 2026-02-13

## TL;DR

This paper proposes a new approach to managing gastric cancer risk after Helicobacter pylori eradication by considering lasting tissue damage and using personalized surveillance strategies.

## Contribution

A novel dual-dimensional framework for post-eradication gastric cancer risk management integrating multidimensional risk assessment and tailored surveillance.

## Key findings

- Residual gastric cancer risk persists after H. pylori eradication due to irreversible mucosal damage and molecular scars.
- A multidimensional risk assessment combining OLGA/OLGIM staging, demographics, lifestyle, and genetics can stratify post-eradication risk.
- Tailored surveillance protocols using AI-assisted endoscopy and molecular biomarkers can improve precision prevention.

## Abstract

Despite the established efficacy of Helicobacter pylori eradication in reducing gastric cancer (GC) incidence, a significant residual risk persists in successfully treated individuals, driven by lasting pathological alterations termed “oncogenic memory,” including irreversible mucosal damage (e.g., intestinal metaplasia), residual pro-inflammatory and epigenetic “molecular scars,” and gastric microbiome dysbiosis. This perspective synthesizes current evidence to advocate for a paradigm shift from a singular focus on pathogen clearance towards a comprehensive, risk-adapted management strategy. We propose a novel, dual-dimensional framework centered on a multidimensional risk assessment that integrates OLGA/OLGIM staging, demographic, lifestyle, and genetic factors to stratify post-eradication individuals into distinct risk categories. The framework subsequently outlines tailored surveillance protocols—specifying endoscopy frequency and advanced biomarker application—leverages technological support from AI-assisted endoscopy and molecular testing, and details differentiated resource allocation models based on regional GC incidence and economic development. This integrated approach provides a practical roadmap for implementing precision prevention, aiming to mitigate the lingering GC risk and ultimately reduce the global disease burden through a dynamic, lifelong management system beyond eradication. To facilitate implementation, we provide a user-ready risk calculator that operationalizes the multidimensional score for cohort-level application.

Graphical summary of the dual-dimensional framework for post-Helicobacter pylori precision prevention. Despite successful H. pylori eradication, residual gastric cancer risk persists due to long-lasting pathological and molecular alterations collectively referred to as oncogenic memory. These include irreversible mucosal damage (e.g., intestinal metaplasia), persistent epigenetic and inflammatory molecular scars, and gastric microbiome dysbiosis. The proposed dual-dimensional management framework integrates a multidimensional risk assessment—encompassing OLGA/OLGIM staging, demographic, lifestyle, and genetic factors—with tailored surveillance protocols, including optimized endoscopy frequency, AI-assisted endoscopic imaging, and application of advanced molecular biomarkers. Furthermore, differentiated resource allocation models are recommended according to regional gastric cancer incidence and economic capacity. This precision prevention approach aims to transform post-eradication management from simple pathogen clearance to a dynamic, lifelong, risk-adapted strategy.Diagram illustrating post-Helicobacter pylori eradication effects and risk-adapted management. The left side shows a stomach with labeled issues: “Oncogenic memory,” “Microbiome dysbiosis,” “Residual molecular scars,” and “Irreversible mucosal damage.” The right panel outlines risk-adapted management, featuring “Multidimensional risk assessment” via OLGA/OLGIM staging, demographic, lifestyle, and genetic factors. “Tailored surveillance protocols” include endoscopy frequency and AI-assisted endoscopy, with “Differentiated resource allocation.” Icons depict related themes alongside text.

Graphical summary of the dual-dimensional framework for post-Helicobacter pylori precision prevention. Despite successful H. pylori eradication, residual gastric cancer risk persists due to long-lasting pathological and molecular alterations collectively referred to as oncogenic memory. These include irreversible mucosal damage (e.g., intestinal metaplasia), persistent epigenetic and inflammatory molecular scars, and gastric microbiome dysbiosis. The proposed dual-dimensional management framework integrates a multidimensional risk assessment—encompassing OLGA/OLGIM staging, demographic, lifestyle, and genetic factors—with tailored surveillance protocols, including optimized endoscopy frequency, AI-assisted endoscopic imaging, and application of advanced molecular biomarkers. Furthermore, differentiated resource allocation models are recommended according to regional gastric cancer incidence and economic capacity. This precision prevention approach aims to transform post-eradication management from simple pathogen clearance to a dynamic, lifelong, risk-adapted strategy.

## Linked entities

- **Diseases:** gastric cancer (MONDO:0001056)
- **Species:** Helicobacter pylori (taxon 210)

## Full-text entities

- **Genes:** COX7A2L (cytochrome c oxidase subunit 7A2 like) [NCBI Gene 9167] {aka COX7AR, COX7RP, EB1, SCAF1, SCAFI, SIG81}, EPCAM (epithelial cell adhesion molecule) [NCBI Gene 4072] {aka Ber-Ep4, BerEp4, DIAR5, EGP-2, EGP314, EGP40}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, RIMS1 (regulating synaptic membrane exocytosis 1) [NCBI Gene 22999] {aka CORD7, RAB3IP2, RIM, RIM1}, PDPN (podoplanin) [NCBI Gene 10630] {aka AGGRUS, D2-40, GP36, GP40, Gp38, HT1A-1}, PROM1 (prominin 1) [NCBI Gene 8842] {aka AC133, CD133, CORD12, MCDR2, MSTP061, PROML1}, SSBP3 (single stranded DNA binding protein 3) [NCBI Gene 23648] {aka CSDP, SSDP, SSDP1}
- **Diseases:** infection (MESH:D007239), carcinogenic (MESH:D011230), intestinal metaplasia (MESH:D007410), gastritis (MESH:D005756), liver cancer (MESH:D006528), mucosal damage (MESH:D052016), gastric microbiome (MESH:D013272), Gastric microbiome dysbiosis (MESH:D064806), Cancer (MESH:D009369), pulmonary nodules (MESH:D055613), atrophy (MESH:D001284), anxiety (MESH:D001007), Atrophic gastritis (MESH:D005757), chronic inflammation (MESH:D007249), dysplasia (MESH:D015792), H. pylori (MESH:D016481), metaplasia (MESH:D008679), GC (MESH:D013274), lesion (MESH:D009059), AI (MESH:C538142), carcinogenesis (MESH:D063646)
- **Chemicals:** N-nitroso compounds (-), alcohol (MESH:D000438), salt (MESH:D012492)
- **Species:** Helicobacter pylori (species) [taxon 210], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

37 references — full list in the complete paper: https://tomesphere.com/paper/PMC12946149/full.md

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Source: https://tomesphere.com/paper/PMC12946149