The classic approach to assess public heath risks is to utilized epidemiology data to identify potential casual agents or factors related to adverse disease outcome. Subsequent hypotheses were evaluated in controlled experimental models, mainly animal studies, leading to detailed relationships of exposure and disease outcome. Subsequently, single variables were altered to identify molecular mechanism. The selection of the model, however, is often crucial to demonstrate the desired effects.

To over come the limitation of ‘selected models’ (inbreed mice strains) it is hypothesized that an outbreed strain of mice, genetically designed to represent a complete intermixed population covering all possible polymorphism, will be an animal model that more closely resembles the human population. High throughput screening of genome, transcriptome, proteome, metabolome, lpipodome, etc and building of complex networks will produce unprecedented knowledge regarding the biology of cells, tissues and organism, including mechanism of diseases development.

As system biology networks being built and validated it is important to elucidate the quantitative effects and relationships of the different variables. Qualitative networks are incomplete models that will certainly be not sufficient to describe complex human populations.  Therefore, to better understand the source of individual susceptibility it is important to determine quantitative relationships between networks nodes to correctly model normal or diseased phenotypes.

Therefore, our research focuses on the interplay between chemical carcinogenesis and nutritional or lifestyle habits, such as diet selection and physical activity. To achieve this we utilize DNA and protein adducts to study carcinogen metabolism, how it is modified by nutritional components and the underlying mechanisms regulating corresponding enzyme activities.