For the last decades cancer therapy was based on the assumption that cytotoxic drugs affect tumor cells due to their high proliferation rate.

It is now generally accepted that cytotoxicity of drugs interacting with DNA is mediated through induction of apoptosis.

The biological ability of a cell to enter the apoptotic pathway in response to DNA damage is determined by the p53 gene.

As a consequence, response to cytotoxic drugs interacting with DNA should depend on the presence of a normal p53 gene.

However, in about 50% of human cancers the p53 gene is defective due to mutation.

Therefore, the status of the p53 gene might be crucial for response to cancer therapy.

We currently test this concept in prospective randomized clinical trials

(see clinical studies).