Helicobacter pylori infection status and evolution of gastric cancer.
10.1097/CM9.0000000000003903
- Author:
Wenlin ZHANG
1
;
Yuxin ZHANG
2
;
Jing NING
2
;
Weiwei FU
2
;
Shigang DING
1
Author Information
1. Department of Gastroenterology, Peking University Third Hospital, Beijing 100191, China.
2. Beijing Key Laboratory for Helicobacter Pylori Infection and Upper Gastrointestinal Diseases (BZ0371), Beijing 100191, China.
- Publication Type:Review
- Keywords:
Autoimmune gastritis;
Bile reflux;
Gastric cancer;
Gastric microbiota;
Host susceptibility;
Inflammation-cancer transformation
- MeSH:
Stomach Neoplasms/genetics*;
Humans;
Helicobacter Infections/complications*;
Helicobacter pylori/pathogenicity*;
Risk Factors
- From:
Chinese Medical Journal
2025;138(23):3083-3096
- CountryChina
- Language:English
-
Abstract:
Gastric cancer (GC) is a globally prevalent malignancy with a particularly heavy burden in China. Helicobacter pylori ( H. pylori ) is a Group I carcinogen for GC, with a higher seroprevalence rate indicating a higher GC incidence. However, only approximately 3% of the individuals with H. pylori infection eventually develop GC, and about 2.6% still progress to GC even 10-20 years after the eradication of H. pylori . Thus, the pathogenic mechanism of H. pylori for GC must be elucidated, and high-risk individuals precisely identified. Furthermore, GC can occur even in individuals who have never been infected with H. pylori . As H. pylori infection rates decline, the proportion of H. pylori -negative GC cases is increasing annually, gaining significant research attention. In this review, potential pathogenic mechanisms of H. pylori infection are explored from the aspects of H. pylori virulence factors and host factors (genetic susceptibility and immune microenvironment). Possible risk factors for H. pylori -negative GC include infections by other microorganisms (e.g., bacteria, fungi, and viruses), autoimmune gastritis, bile reflux, genetic mutations, and environmental factors. We aim to review the potential mechanisms for GC with varying H. pylori infection statuses, identify the high-risk individuals, and pose questions that need to be addressed. In the future, as the prevalence of H. pylori infection gradually decreases, GC prevention and management must evolve to address host-specific factors and the growing challenge of H. pylori -negative GC by integrating multidisciplinary perspectives.
