Chances are slim that mutations accumulate in individual somatic cells and their progeny to make up a significant tumour mass since cellular repair programs exist to prevent this scenario from happening.Errors can also occur beyond DNA replication such as during transcription or translation when proteins are made, and when they are activated, shut off or recycled.Besides hyperactive oncogenes, defects in tumour suppressor genes can also contribute to carcinogenesis.
To deliver optimal and personalized cancer prevention and treatment programs to the people, more than information on the DNA level are required.
The DNA is the blueprint of life, but we have to know how the individual bricks, the proteins, are fitting together.
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.
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.
Neighbouring cells can directly interact and alter intracellular signal transduction by secreted messenger molecules or membrane-anchored ligands and respective receptors.
The numbers and different types of cells within a local niche in the human body depend on the lifestyle of the entire organism.
There is accumulating evidence that our genes do only partially determine our fate.
Our understanding of how our lifestyle affects human health mechanistically is still in its infancy.