Epigenetic Regulation in Environmental Diseases

Epigenetic Regulation in Environmental Diseases research focuses on deciphering how environmental stressors alter the epigenome via DNA methylation and induce chromatin remodeling which results in cancer or other chronic diseases. Our research findings may lead to the development of improved preventive measures and therapeutic strategies to reduce the burden of these chronic diseases. In the Department of Environmental Health and Engineering, our goal is to translate scientific findings providing disease management recommendations to improve public health.

Epigenetics Explained in Five Minutes: "Environment, Epigenome, and Public Health"

Research Highlights

Translating Epigenetic Studies to Human Population Studies

Results from the epigenetic studies in laboratory can be further validated in populations. We have documented how inter-individual epigenetic variations affect disease risk in response to environmental exposures not limited to traffic-related air pollutants, heavy metals, and endocrine disrupting chemicals.

Environmental Exposure and Disease Pathogenesis

Susceptibility of disease was believed to be determined solely by genetic variations causing dysregulation of gene expression that underlies the genesis of disease. However, it has recently become clear that epigenetic disruption of gene expression plays an equally important role as genetic variations in the development of disease. Epigenetic reprogramming becomes one of the determinant of origins of human disease as there is a relatively long gestation, a period of postnatal and perhaps life-time allow for prolonged interactions with the environment. It is believed that genes altered by environment may be "transmitted" to next generation via epigenetic alteration. Utilizing the experimental models, we demonstrated the epigenetic effects of xenoestrogens and air pollutants on carcinogenesis and asthma pathogenesis.

Epigenomics

To further our understanding in epigenetic changes and environmental diseases, we aim to determine how epigenetic codes, including patterns of DNA methylation and combinatorial patterns of simultaneously occurring histone modifications, are established and how this establishment goes awry upon environmental stimuli, thus contributing to human diseases. Susceptibility of disease was believed to be determined solely by gene mutations, deletions, gene fusion, tandem duplications, or gene amplifications causing dysregulation of gene expression that underlies the genesis of disease. However, it has recently become clear that epigenetic disruption of gene expression plays an equally important role in the development of disease. Epigenetic reprogramming becomes one of the determinant of origins of human disease as there is a relatively long gestation, a period of postnatal and perhaps life-time allow for prolonged interactions with the environment including hypo- or hyper-nourishment, infection, hormonal, drug, or toxin exposures. It is believed that genes altered by environment may be "transmitted" to next generation via epigenetic alteration.

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