Reparaturwege in Krebszellen gezielt ausschalten

Mutations in BRCA1 or BRCA2 are associated with breast, ovarian and other cancers. Cells with these mutations are defective in homologous recombination (HR), one of two main processes to repair DNA double-strand breaks (DSBs). Survival of these cells strongly relies on the usage of alternative repair pathways, such as POLθ-mediated end-joining (TMEJ). Thus, targeting TMEJ could be a promising new strategy for the therapy of BRCA1- and BRCA2-mutant tumours.