ReviewFrontiers in immunology2026
The inflammation-epigenetics axis in gastric cancer: Helicobacter-driven field defects, immune escape, and therapeutic frontiers.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Gastric cancer provides a clinically relevant model of the inflammation-epigenetics axis because Helicobacter pylori can drive prolonged mucosal inflammation before malignant transformation. Inflammatory signaling remodels DNA methylation, histone states, chromatin accessibility and RNA-regulatory programs, generating epigenetic field defects that may persist after bacterial eradication. Epstein-Barr virus-positive gastric cancer represents a distinct hypermethylated and immune-adapted state. We organize these processes using four coordinates: inflammatory driver, dominant epigenetic lesion, cellular compartment and reversibility. Across gastric cancer subtypes, epigenetic plasticity contributes to field cancerization, antigen-presentation loss, epithelial-mesenchymal transition, stemness and drug-tolerant persistence, while parallel reprogramming of immune and stromal compartments promotes treatment resistance. Tissue and circulating DNA methylation currently have stronger translational support than circulating non-coding RNA or m6A-based signatures, which remain investigational because of source attribution, assay standardization and validation limitations. Therapeutic translation should therefore combine removal of the sustaining inflammatory driver with biomarker-guided epigenetic priming and state-matched immune or stromal intervention. Longitudinal and externally validated studies are required to convert these mechanisms into clinically useful biomarkers and treatment strategies.
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