Oxidants at the Epigenetic Crossroads: How Chronic Inflammation Writes the Cancer Script

The review by Damiano et al. [1] synthesizes a large body of work, arguing that oxidants produced during chronic inflammation can actively reshape deoxyribonucleic acid (DNA) methylation landscapes and thereby contribute to carcinogenesis rather than merely cause random genetic damage.The authors highlight the fact that ~20% of human cancers arise in chronic-inflammation settings and propose that immune cell-derived reactive oxygen species (ROS) are an underappreciated mechanistic bridge between persistent inflammation and the aberrant methylation patterns typical of tumors.