The focus of our molecular epidemiology laboratory is to understand complex interactions between environment and genome/epigenome in contribution to human diseases.  We are performing functional epi/genetic analyses in population studies to elucidate disease mechanism and to identify/validate biomarkers for disease risk or prognosis. Such work is of great importance in identifying disease-causing exposure, clarifying disease etiology, designing prevention strategies through lifestyle modifications, and even assisting disease treatment and management.

We have three active research tracks in the lab:

(1)    Environmental epi/genetics in breast cancer.

We have been working extensively to elucidate the effects of environment (endocrine disruptors) and lifestyle (dietary intake) on breast cancer via epigenetic mechanisms. We incorporate environmental measurements (questionnaire, biomarkers), genomic/epigenomic tools (gene expression, SNPs, methylation, and microRNAs), and bioinformatics into large epidemiologic studies.  Given that cancer is considered a “developmental disease”, we are using a translational approach, combining animal and population studies, to systematically evaluate the role of endocrine disruptors (chemicals found ubiquitously in the environment) in breast cancer etiology during different stage (windows of susceptibility) of breast development.

(2)    Environmental Epi/genetics in Reproductive Health and Child Development.

We use placenta as our model system. As an interface between maternal and fetal environment, placenta is the source of fetal nutrients and immune regulation as well as a barrier for environmental toxins; these effects are modulated by simultaneous production of many pregnancy related hormones, proteins and growth factors thereby fulfilling a critical role in proper intrauterine development.  Thus placenta plays a vital role in productive health as well as fetal growth and neurodevelopment.  We are actively studying the role of placental genome and epigenome, such as genomic imprinting, in birth outcomes and child neurodevelopment.  We are also studying the environmental influences, such as maternal stress, nutrition and chemical exposure, on the placental epigenome. Utilizing resources of several birth cohorts, we are trying to build a comprehensive model to examine the inter-relationships among in utero environment, placental epigenome, and fetal growth and neurobehavioral outcomes. 

(3)    Developmental Origins of Human Diseases.

The Developmental Origins and Health and Disease (DOHaD) hypothesis posits that lifelong health is partially shaped by the environment experienced during early developmental period. We are investigating this hypothesis in two exposure - disease models.  The first model is endocrine disruptors and breast cancer in which are conducting trans-disciplinary studies combining animal and human studies to systematically evaluate the role of endocrine disruptors in breast cancer etiology during different stage of breast development. The second focuses on adverse maternal environment during pregnancy (maternal stress, toxin exposure) and neurodevelopment of the children in which we are conducting genetic and epigenetic profiling of the placentas and cord bloods.