Publication at First Faculty of Medicine |
2015
Abstract
The search for cellular processes that may serve as targets for targeted therapy is also concentrated on DNA repair mechanisms. Up to half of ovarian carcinomas are defective in homologous recombination, one of the pathways of DNA repair.
Disabling base excision repair (BER) mechanism via poly(ADP-ribosa)polymerase (PARP) inhibition leads to increased cancer cell sensitivity to chemotherapy or directly to the so-called synthetic lethality. Currently, olaparib has been approved for the treatment of recurrent platinum-sensitive high-grade serous ovarian carcinoma in patients with proven germ-line or somatic mutation in either BRCA1 or BRCA2.