Complex human diseases arise from the interaction between many different genes and the environment and are the main causes of death in Europe. Up to 60% of the adult population dies from complex diseases such as cancer and diseases of the circulary system.
In contrast to the successful identification of genes underlying rare monogenic diseases, studying the genetic basis of common complex diseases has been more challenging. Evidence is mounting to suggest that the genetic background or genotype (i.e. the genetic make-up of all alleles at all loci) has a profound impact on a wide variety of complex disease phenotypes and signaling pathways. But so far, the genetic mechanisms underlying these modifiers are unknown.
The nematode worm Caenorhabditis elegans is an important model for the identification and characterization of genes underlying complex diseases in humans. The worm has been studied widely for biomedical research, especially in the functional characterization of novel drug targets which can be translated for human health.
Within PANACEA we will use C. elegans to address the following two key questions:
- how the genetic background affects complex disease signaling pathways
- whether we can predict the effect of the genetic background on these pathways