Some anti-cancer treatments not only target tumour cells but also healthy cells. If their effects on the latter are too strong, their use can become limiting.
Mar 20 2024University of Geneva Some anti-cancer treatments not only target tumor cells but also healthy cells. If their effects on the latter are too strong, their use can become limiting. A team from the University of Geneva , in collaboration with Basel-based FoRx Therapeutics, has identified the mechanism of action of PARP inhibitors, used in particular for breast and ovarian cancer in patients carrying the BRCA gene mutation.
Non-cancerous cells killed by treatments PARP inhibitors have been used to treat this type of cancer for around 15 years. PARP proteins can detect breaks or abnormal structures in the DNA double helix. PARPs then temporarily stick to the DNA, synthesizing a chain of sugars which acts as an alarm signal to recruit the proteins involved in DNA repair. Treatments based on PARP inhibitors block these activities and trap the PARP protein on the DNA.
The mechanisms by which anti-PARP drugs kill cells are still poorly understood. Professor Thanos Halazonetis' laboratory in the Department of Molecular and Cellular Biology at the UNIGE Faculty of Science, in collaboration with FoRx Therapeutics, has dissected the mechanisms of action of PARP inhibitors.
Michalis Petropoulos, post-doctoral fellow in the Department of Molecular and Cellular Biology at the UNIGE Faculty of Science and first author of the study
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