| Popis: |
DNA is the principal target of many conventional anticancer agents, and inhibition of DNA repair is one of the most promising strategies in novel cancer therapy. Many studies demonstrated that nonhomologous end-joining (NHEJ) repair pathway proteins, and especially DNA-dependent protein kinase (DNA-PK), is an attractive and effective target for the sensitization of cancer cells, including the most common type of leukemia in western countries, chronic lymphocytic leukemia (CLL), to DNA double-strand break (DSB)-inducing agents used in conventional cancer therapy. Nevertheless, promising results obtained in vitro cannot be translated to the clinic yet due to the nature of the DNA-PK inhibitors which are either nonspecific, for the first class of inhibitors, or degraded/eliminated from the human body before reaching the tumor site for the newer specific DNA-PK inhibitors. |
