Researchers discover a new therapeutic target for the treatment of malignant melanoma

Malignant melanoma is one of the most deadly cancers in the Western world. Although effective drugs are available, initial treatment success is almost consistently followed by the emergence of resistant cancer cells. Researchers at the Institute of Biochemistry have successfully overcome drug-resistance in malignant melanoma cells. Their findings have been published in the prestigious medical journal Oncogene.

One of the reasons why malignant melanoma is considered one of the most aggressive forms of cancer is the fact that tumors measuring as little as 0.7 mm can give rise to metastases in other organs such as the liver, lung and brain. Once the tumor has spread, the chances of recovery are very slim. The rate of new cases of malignant melanoma is increasing at a dramatic rate worldwide. Even young people under the age of 40 are commonly affected. The main risk factors are excessive sun exposure, sunburn and genetic predisposition.

Adaptable cancer cells

While certain melanomas with a specific gene mutation respond well to targeted therapeutics, in nearly all cases, the promising initial results unfortunately quickly turn to disappointment. Cancer cells often quickly become resistant to treatment and the tumor continues to spread, sometimes even more rapidly and aggressively than before. Scientists suspect that during treatment, cancer cells learn how to survive and even thrive under different conditions.

A team of scientists working with Prof. Dr. A. Bosserhoff and Dr. P. Dietrich, from the Chair of Biochemistry and Molecular Medicine, and Prof. Dr. C. Hellerbrand, who holds a Professorship in Biochemistry and Molecular Pathobiology, have now found a way to prevent drug resistance in melanoma cells. It turns out that, during chemotherapy, skin cancer cells produce increasing amounts of a protein known as KRAS. This protein activates specific cell signalling pathways, which allows the tumor to survive and continue to spread despite treatment.

A stop sign for a cancer cell gene

The key to success lies in the inhibition of KRAS. The researchers successfully switched off cellular KRAS synthesis, allowing cells to respond to treatment. They also used a new KRAS inhibitor developed in Germany.

This compound, which is called Deltarasin, causes skin cell apoptosis and overcomes treatment resistance. Its effects are multiplied when used in combination with conventional drugs.

Dr. P. Dietrich explains. Prof. Dr. A. Bosserhoff is similarly convinced of the promise of the drug:

The approach has a great deal of potential and is being developed further. In the meantime, FAU has applied for a patent for this discovery.

Further information

Prof. Dr. Anja Bosserhoff
Phone: +49 9131 8524190
Dr. Peter Dietrich
Phone: +49 9131 8529384

Category: News, Research