|My laboratory investigates the response of individuals or populations to toxic or carcinogenic environmental agents. The long-term objective of this work is to elucidate the molecular mechanisms that underlie this response. Many chemical compounds interfere with the control mechanisms that regulate gene expression causing the overexpression of some genes and the repression of others. The ultimate effect of this process is an alteration of the steady-state levels of the proteins encoded by the genes affected. Potentially, if exposures to the agents occur during embryonic development, their ultimate effect may be the sensitization of the organism to develop adult diseases. In recent years, it has become increasingly clear that fetal exposure to environmental agents is indeed one of the major causes of environmental disease in the adult. My interests are centered, on the one hand, on the molecular mechanisms of action of several toxic environmental agents, including the dioxins and several heavy metals, and on the other, on the analysis of epigenetic responses to these agents as they interact with environmentally relevant genes. The genes on which we focus this work are those that respond transcriptionally to activation of the aryl hydrocarbon receptor, a transcription factor with a regulatory role in the expression of detoxification enzymes that also functions as a cell cycle environmental checkpoint. We are actively studying the molecular mechanisms associated with disruption of chromatin remodeling when gene induction is derailed by exposure to mixtures of carcinogenic polycyclic aromatic hydrocarbons and heavy metals. In this regard, my interests are focused on the analysis of chromatin modifications taken place during differentiation that are derailed by environmental exposure.