The development of cancer is the result of changes to the genome of a single cell. Most mutations in the genome are repaired by the cells immediately, without permanent damage. If the cells fail to repair the damage, it may lead to a change in the characteristics of the cell, ultimately developing into a tumor.
For instance, if the change results in the inactivation of a tumor suppressor gene, which guards the cell against uncontrolled division, the cell may become cancerous. Even small changes to the genome can cause this characteristic change.
If DNA repair mechanisms and regulation of cell growth and division are damaged, the cell will begin to divide uncontrollably, and a tumor will form. Over time, the tumor cells accumulate further mutations; they diverge from their original function and ignore regulatory mechanisms. This then leads to an increase in the ability for daughter cells to grow in other tissues, called metastasis.
The cell is genetically altered by external or internal influences (e.g., radiation exposure, smoking, sun exposure).
The genetically modified cell begins to divide under weaker control.
The tumor grows and gathers further genetic alterations.
The tumor cells are now able to establish themselves outside their original tissue and grow there. They form metastases.
How we can help you
Cancers, in particular, require a rapid and targeted therapy in order to best exploit the chances of successful treatment. As time goes on, more and more drugs are available that act precisely on specific genetic mutations present within the tumor cells. Previously, cancer diagnostics analyzed only a few commonly occurring genomic alterations with respect to the specific tumor type; however, it is now clear that every tumor is different, and each may be uniquely susceptible to different drugs via specific genetic mutations, which would not have been previously contemplated. A comprehensive genetic study of the tumor can thus help select the most promising drug against the cancer of a patient.
Our panel of somatic tumor genes comprises 742 genes that may contribute to tumorigenesis. Furthermore, selected chromosomal translocations are examined in 31 additional genes. For analysis, both tumor tissue and normal tissue of the patient are required (preferably blood or skin tissue). The identification of somatic mutations allows a more precise diagnosis of tumor diseases and can thus support the selection of an appropriate therapy.