# Managing dangerous liaisons: lessons from Helicobacter pylori for understanding bacterial carcinogenesis

**Authors:** Jazmine A. Snow, Stavroula K. Hatzios, Nina R. Salama

PMC · DOI: 10.1128/jb.00457-25 · Journal of Bacteriology · 2026-01-15

## TL;DR

This paper reviews how Helicobacter pylori, a bacterium linked to stomach cancer, has helped scientists understand how chronic infections can lead to cancer.

## Contribution

The paper emphasizes the use of mouse models and recent findings on H. pylori's adaptation to oxidative stress in studying bacterial carcinogenesis.

## Key findings

- H. pylori's virulence factors like VacA and CagA contribute to gastric disease and cancer.
- Mouse models are crucial for replicating H. pylori-driven human disease mechanisms.
- H. pylori's adaptation to oxidative stress enhances its role in promoting cancer.

## Abstract

As the first bacterium to be deemed a class I carcinogen by the World Health Organization in 1994, Helicobacter pylori has paved the way for studying complex host-pathogen interactions. While 1982 marked the discovery of this helical-shaped microorganism found in gastric biopsies by Drs. Robin Warren and Barry Marshall, it took years to link H. pylori infection to gastric inflammation, ulcers, and adenocarcinoma (recognized by a Nobel Prize in 2005). Further investigations into how H. pylori colonizes the stomach, the identification of key virulence factors (such as VacA, CagA, and outer membrane proteins), and global epidemiological studies solidified the impact of H. pylori on gastric disease. This review details the seminal discovery of H. pylori and subsequent work that cemented its status as a microbial carcinogen. Because chronic H. pylori infection and progressive changes to the tissue environment prior to cancer development can span years/decades, studying H. pylori pathogenesis has been challenging. We focus on the importance of using animal models, in particular mouse models, to recapitulate hallmarks of H. pylori-driven human disease. Finally, we highlight recent findings illustrating how H. pylori has adapted to survive and utilize oxidative stress induced during infection, which potentiates cancer development. Due to the long-lasting nature of H. pylori infection and associated remodeling of the host environment that, in turn, promotes carcinogenesis, H. pylori stands as a model organism for understanding other chronic bacterial infections in humans and pathogen-associated malignancies.

## Linked entities

- **Proteins:** vacA (prohibitin domain-containing protein), S100A8 (S100 calcium binding protein A8)
- **Diseases:** ulcers (MONDO:0043839), adenocarcinoma (MONDO:0004970)
- **Species:** Helicobacter pylori (taxon 210), Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** VacA [NCBI Gene 48201093], CagA [NCBI Gene 48200769]
- **Diseases:** carcinogenesis (MESH:D063646), gastric inflammation (MESH:D007249), gastric disease (MESH:D013272), H. pylori infection (MESH:D016481), adenocarcinoma (MESH:D000230), cancer (MESH:D009369), ulcers (MESH:D014456), bacterial infections (MESH:D001424), infection (MESH:D007239)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090], Helicobacter pylori (species) [taxon 210]

## Full text

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## Figures

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## References

273 references — full list in the complete paper: https://tomesphere.com/paper/PMC12918743/full.md

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Source: https://tomesphere.com/paper/PMC12918743