There is accumulating evidence that our genes do only partially determine our fate.
Smoking does not only correlate with the incidence rate of lung cancer, there is a causal relationship.
Tobacco smoke creates polycyclic aromatic hydrocarbons, which interfere with DNA thereby causing mutations that perturb the fine balance of physiological processes in the cells of our body.
Besides hyperactive oncogenes, defects in tumour suppressor genes can also contribute to carcinogenesis.
It is the dynamic interaction between numbers of genetic elements that causes transformation of healthy cells.
The ability of a cell to sense growth factor signals depends also on the cellular microenvironment.
Cells in the proximity can take up growth hormones thereby preventing the exposure of other cells to those soluble factors.Not only protein-coding sequences are relevant in this respect.In fact, the “non-coding” DNA constitutes 98% of our genome and as such contributes to the regulatory complexity of the human DNA. All these aspects also apply to the modern life sciences. Innovation creates new scientific disciplines, which have never existed before.If only a single gene existed that caused cancer, one would just need to identify this individual oncogene to combat the tumour.Yet, we are lacking a mechanistic understanding of the processes that trigger the onset of different tumours.While causes of carcinogenesis are still under debate, the fatal consequences are widely accepted: cellular transformation, tumour growth and formation of metastases. Since the breakthrough in the Human Genome Project in 2001, the focus shifted to the systematic study of the complex interplay between all genes of an organism. During the last decades of the previous century it was still sufficient for academic success to characterize a single gene in a model system.Mutations are not restricted to a single gene within an individual cell type.Many positions in the genome can be affected by mutations with severe consequences for the equilibrium state of entire cell populations.