Epidemiological and animal data suggest that chemicals with the potential to mimic endogenous hormones may be involved in the development of hormone-dependent as well as other cancers and that the initiation occurs at early life stages. However, the evidence for a causal association between exposure to endocrine disruptors during early life stages and increased risk of subsequent cancers is scarce and need further research.
In this project we hypothesize that mixtures of potential hazardous chemicals contribute to the documented temporal and spatial increase in cancer incidence. To assess a potential link between developmental exposure and increased risk of cancers, we will use two in vivo (animal) models to assess whether dietary environmental chemicals contribute to the induction of colorectal cancers and to identify potential underlying mechanisms focusing on the following hypotheses:
1. Exposure to POPs increase the risk of colorectal cancer.
2. Exposure to POPs during early life stages (fetus to pre-puberty) increase the susceptibility to develop cancer compared to adult exposure only.
3. Colorectal cancer may be induced by nuclear receptor signaling.
The project will use established state of the art tools including genetic modified animal models and omics methods to generate new knowledge of importance for cancer research, and will promote and foster collaboration between cancer researchers and toxicologists.