부산대학교 도서관

Epigenomic alterations are one of the causes of carcinogenesis, and are likely to be involved in allergies, autoimmune disorders, and type 2 diabetes. It is now well-established that driver mutations and epigenomic alterations occur in epithelial cells in normal-appearing tissues, which can produce the “field for cancerization.” We previously demonstrated that chronic inflammation induced aberrant DNA methylation in epithelial cells, and that its severity was correlated with cancer risk. Recently, we found that aberrant DNA methylation was also induced by aging and chronic inflammation in mouse gastric fibroblasts. In human gastric fibroblasts, increased H3K27 acetylation by hypoxia was observed in the HIF1A-target enhancers. These suggest that biological responses to the intrinsic and extrinsic factors, including chemicals and foods, induce epigenomic alterations in epithelial cells and fibroblasts in nonmalignant tissues. In tumors, endothelial cells and immune cells are known to exhibit phenotypic changes with epigenomic alterations and enhance metastatic ability and therapy resistance. Therefore, it is important to accelerate the study on how to detect the lifestyle factors that alter epigenome of an ecosystem in nonmalignant tissues.