Tumors develop from cells as a consequence of changes in genes, called mutations. These changes happen by chance and normally are corrected by the cell’s DNA repair systems. Exposure to carcinogens, such as tobacco smoke or UV radiation, increases the number of mutations. A not correctly repaired mutation can lead to cancer. These obtained mutations are called somatic mutations. Cancer promoting somatic mutations result in changed protein functions leading to dysregulated cellular processes. Initially, these genetic changes promote loss of growth control in affected cells during cell division. Additional mutations select for cell clones which successfully continue proliferation and decrease their rate of death. Further mutations accumulate in the course of tumor progression and promote tumor cell distribution to distant organs (metastases). The somatic mutations which are acquired by tumors in the course of the disease are individual and differ not only between different cancer entities but also from patient to patient. Thus, cancer is a multifactorial and heterogeneous genetic disease.
Every tumor is unique.
The individual set of tumor-specific mutations helps the tumor to survive, reduce sensitivity to treatment, and develop resistance against therapeutic agents. Knowing the somatic mutations helps to identify promising therapeutic strategies and to avoid ineffective treatment options with their associated side effects. Currently, anti-cancer therapies are still mostly chosen based upon the organ of origin. However, studies show that comprehensive genetic tumor diagnostics provide therapeutically relevant information in over 76% of all tested cases (Frampton et al., 2013; CeGaT internal data).