Helicobacter pylori-Induced Inflammatory Cancer Transformation Microenvironment Drives Gastric Carcinogenesis - PubMed
5 hours ago
- #Cancer-associated fibroblasts
- #Helicobacter pylori
- #Gastric cancer
- H. pylori eradication reduces gastric cancer risk but has limited effect on advanced atrophic gastritis.
- A persistent inflammatory-cancer-transformation microenvironment (ICTM) drives gastric carcinogenesis post-eradication.
- Single-cell atlas analysis reveals distinct epithelial trajectories in post-eradication patients with or without pathological improvement.
- Immunomodulatory cancer-associated fibroblasts (iCAFs) promote epithelial malignancy and immunosuppression.
- CCN2+ iCAF1 and C3+ iCAF3 subtypes persist in post-eradication CAG patients and contribute to malignant transformation.
- H. pylori infection reprograms iCAFs, leading to extracellular matrix reorganization and senescence with SASP.
- Infection-driven iCAF-epithelial niche reprogramming creates an immunosuppressive state post-eradication.
- Specific iCAF subtypes are potential therapeutic targets for post-H. pylori eradication therapies.