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  • Friday, April 29, 2016
  • 1:30 PM–2:30 PM
  • Science Building 010

Peter Dornbos, doctoral student in Biomedical Toxicology, Michigan State University

Approximately 99.9% of the 3 billion base pairs of the human-genome are identical between any two individuals. The differences in genetic sequence between individuals amount to approximately 3 million base pairs. Such differences provide the diversity we see across the human population. Genomic variation is inherently a good thing as it improves overall fitness; such, a small change in an environmental niche will not be detrimental to a species as a whole.  However, from a toxicologist’s standpoint, such genomic variation is source of uncertainty. Variation ultimately translates to differences in response to chemicals, whether it be a pharmaceutical or a hazardous pollutant in the environment. Traditionally, genetic variation is avoided within the basic sciences as it complicates the understanding of the biological mechanisms that drive phenotypic responses. Thus, the majority of data available regarding chemical hazards has been collected using genetic clones, such as inbred rodent strains and cell lines. From the standpoint of assessing the risk posed by chemical exposures, understanding the variation in response throughout the population is absolutely essential. In this seminar, I will discuss the method behind assessing risk for chemical exposures in the human population. I will also discuss and show some results from a human and mouse model used by our laboratory to assess the impact of population diversity on variability inherent in the response to an environmental toxicant called 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Finally, I will discuss some future research directions in our lab and in the field of toxicology and risk assessment. 

April 2016
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