For quite some time it has been known that a genetic modification of the p53 tumour-suppressor gene (TP53) in a tumour does not bode well for the patient. However, just why this is the case, has now been identified at the Medical University of Vienna.
The research team headed by Univ. Prof. Dr. Daniela Kandioler has been able to demonstrate how dramatically the efficacy of numerous chemotherapeutic substances are influenced by the tumour’s p53 gene status. Between 1999 and 2013, the p53research research group investigated the impact of the p53 gene status on the responses to therapy in more than 1,000 cancer patients. The Mark53 clinical studies have demonstrated, among other things, that frequently applied chemotherapies are significantly more effective among patients with a normal p53 gene status than was previously thought, whilst the same chemotherapy had a negative impact on patients with a mutated p53gene status.
These results were endorsed among patients with lung cancer, breast cancer, oesophageal cancer, colon cancer and liver metastases and ought to be relevant for ovarian cancer too. In other words – with the aid of the TP53 biomarker- the cancer therapy can be tailored to all of the most frequently occurring cancer types.
A p53-adaped cancer therapy improves the efficacy of the cancer therapy and simultaneously reduces patient risk.