improve science, health and society
Our commitment does not stop with science at the basics; we bring our results all the way to the patients. The Helleday Laboratory focuses on harnessing defects in the DNA damage response and metabolism to develop novel therapies. The group is behind several success stories such as the synthetic lethal concept of treating BRCA mutated cancers with PARP inhibitors.
We are happy to have had Katharina visit our lab. Listen to her story!
Biochemistry, assay development and in vitro pharmacology. Disease Models and Tissue Handling.
DNA damage and repair in cancer, DNA replication, repair and transcription, metabolism.
The Helleday Laboratory consists of a large team of mixed professions from industry and academia; basic molecular biologists, medicinal chemists, pharmacologists, biochemists and practicing clinicians, amongst others. What brings us together is our dedication to make our basic science discoveries reach all the way to help patients to improve their quality of life.
The Nobel Prize laureate Otto Warburg who pioneered cancer metabolism research once said that
“The cure of human cancer will be the resultant of biochemistry of cancer and of biochemistry of
man “. We could not agree more. With today’s molecular knowledge of altered DNA damage
response (DDR) and metabolic pathways in cancer cells we are making real advances in progressing
cancer treatments. Read about how we target DDR and nucleotide metabolism.
Chemo- and radiotherapy remain as the backbone of cancer treatments, and they work by causing
damage to the cancer cell’s DNA. We know today that cancer cells have a high load of DNA damage
as compared to normal cells. The Helleday lab identify ways to inhibit DNA repair that selectively kills
cancer or disease cells without harming normal cells. The most renown example is that of using PARP
inhibitors to selectively kill recombination defective cancers, such as inherited breast- and ovarian
cancer. Let us show you many more examples that is in or soon entering the clinic.