{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T11:03:36Z","timestamp":1789556616740,"version":"build-2803163510"},"reference-count":72,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T00:00:00Z","timestamp":1789516800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Gastric cancer provides a clinically relevant model of the inflammation\u2013epigenetics 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\u2013Barr 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\u2013mesenchymal 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.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1955428","type":"journal-article","created":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T10:19:22Z","timestamp":1789553962000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["The inflammation\u2013epigenetics axis in gastric cancer: Helicobacter-driven field defects, immune escape, and therapeutic frontiers"],"prefix":"10.3389","volume":"17","author":[{"given":"Yue","family":"Bai","sequence":"first","affiliation":[{"name":"Combined Ward of Traditional Chinese and Western Medicine, Shengli Oilfield Central Hospital","place":["Dongying, Shandong, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhongran","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Shengli 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