IL1B
Overview
IL1B encodes Interleukin-1 Beta, a pro-inflammatory cytokine central to the innate immune response. In the stomach, H. pylori infection triggers IL-1β release, which can drive CDH1 promoter methylation in gastric epithelial cells and amplify atrophic gastritis, thereby increasing gastric cancer risk.
Alterations observed in the corpus
- H. pylori-induced IL-1β drives somatic CDH1 promoter methylation in gastric epithelial cells, phenocopying germline CDH1 loss-of-function and contributing to diffuse gastric cancer development. PMID:24816255
- High-responder IL1B cytokine polymorphisms amplify H. pylori-driven atrophic gastritis and intestinal metaplasia, increasing gastric cancer risk in familial aggregation contexts. PMID:24816255
Cancer types (linked)
- STAD (gastric adenocarcinoma): IL1B acts both as an epigenetic modifier (CDH1 methylation) and a low-penetrance susceptibility variant relevant to familial non-hereditary gastric cancer (FNHGC). PMID:24816255
Co-occurrence and mutual exclusivity
- Co-listed with IL10 and TNF as pro-inflammatory cytokine polymorphism loci contributing to H. pylori-driven gastric carcinogenesis. PMID:24816255
Therapeutic relevance
- H. pylori eradication is the primary intervention; eradication reduced GC risk by 55% in family-history carriers in a landmark RCT, thereby mitigating IL-1β-driven epigenetic damage.
Open questions
- The relative contribution of IL1B-driven CDH1 methylation vs. direct H. pylori cytotoxic damage vs. immune-mediated mucosal injury in FNHGC initiation is unresolved.
Sources
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