Introduction

Carcinogenesis has historically been viewed as a disease resulting from genetic mutations occurring in a particular order with possible selective stimulation of these mutated cells to grow. This multistage theory of carcinogenesis has formed the basis for much of our understanding of the cancer process and has stimulated many of the experimental methods used to assess cancer risks. Only recently have researchers begun to focus on the effects of secondary pathways on the initiation, progression, and promotion of carcinogenesis. One area receiving considerable attention is the impact of modifications of endocrine hormones on cancer risks.

Genomic and non-genomic endocrine signaling pathways are extensively present in the body and function in a complicated manner. Receptors, ligands, enzymes, proteins, and catalysts work together closely within the same cell and between different cells and organ systems. By means of this direct and indirect signaling, a more or less homeostatic state is preserved. At this moment, it is still not clear on how this closely regulated system is affected by an exogenous agent.

Increasing interest in this area of research arose after epidemiological studies identified a significant increase in the incidence of hormone-dependent diseases including cancers of the breast, prostate, and testis, and suggested that environmental factors may contribute to this increased incidence.

Development of cancers can be influenced by exposure to estrogens or estrogenic drugs. This has been demonstrated through experimental initiation/ promotion studies [1], epidemiology studies [2], and efficacy of hormone agonists in treating cancers. It is possible that estrogen-like compounds such as di-ethylstilbestrol, DDT, dioxins, and bisphenol A could yield similar results. Widespread exposure and the commercial significance of many of these agents have made endocrine-disrupting chemicals a contentious health concern and environmental issue.

Focused studies on the potential for toxicity from endocrine active compounds is a fairly new field of scientific research. Much of the research in this area has derived from mainly two factors that developed exponentially in the last few decades. The first is molecular biology. There have been substantial gains in our understanding of receptor binding, interaction, signaling pathways, and compounds involved in these processes. This research has explored down to the level of receptor-types, genetic background, genomic and non-genomic interactions. The second factor is an enormous increase in "desk" computing power, making it possible for a scientist to run complicated biomathematical models, to analyze and test effects resulting from a particular intervention. The challenge for the coming years is to combine these two aspects. This combination is only possible when both sides work together. Molecular biologist and toxicologists need to understand why mathematical modeling is important and helps in exploring new directions of their own research field. And mathematicians must make great strives to fully understand the biology, focusing on mechanistic/physiologically based models. Only through the integration of information can a true, mechanism-based approach to risk assessment be achieved. What follows is a discussion of this approach, weighing heavily on our experience of modeling the estrogen cycle in mammalian systems.

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