| Autor: |
Shilkin ES; Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, 123182, Russia., Boldinova EO; Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, 123182, Russia., Stolyarenko AD; Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, 123182, Russia., Goncharova RI; Institute of Genetics and Cytology, National Academy of Sciences of Belarus, Minsk, 220072, Republic of Belarus., Chuprov-Netochin RN; Moscow Institute of Physics and Technology, Dolgoprudny, Moscow Region, 141701, Russia., Smal MP; Institute of Genetics and Cytology, National Academy of Sciences of Belarus, Minsk, 220072, Republic of Belarus. m.smal@igc.by., Makarova AV; Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, 123182, Russia. amakarova-img@yandex.ru. |
| Abstrakt: |
Many chemotherapy drugs block tumor cell division by damaging DNA. DNA polymerases eta (Pol η), iota (Pol ι), kappa (Pol κ), REV1 of the Y-family and zeta (Pol ζ) of the B-family efficiently incorporate nucleotides opposite a number of DNA lesions during translesion DNA synthesis. Primase-polymerase PrimPol and the Pol α-primase complex reinitiate DNA synthesis downstream of the damaged sites using their DNA primase activity. These enzymes can decrease the efficacy of chemotherapy drugs, contribute to the survival of tumor cells and to the progression of malignant diseases. DNA polymerases are promising targets for increasing the effectiveness of chemotherapy, and mutations and polymorphisms in some DNA polymerases can serve as additional prognostic markers in a number of oncological disorders. |
