Analysis of thermoradiosensitization using radiation repair deficient cell lines

Full text: Cell lines having wild type parent cells and derived mutant radiation repair deficient cells were evaluated to determine if specific repair deficiencies could influence thermoradiosensitization. In mouse cells that had DNA polymerase β knockout and in human breast carcinoma cells transfected with the DNA polymerase β gene to give elevated expression, no difference was observed in thermoradiosensitization compared to the parental cell lines. These results indicate that DNA polymerase β and the BER pathway are likely not involved in thermoradiosensitization. Using mouse embryo fibroblasts MEF and the KU70 knockout derivative cell line we found that there was thermo radiosensitization in both lines, thus the non homologous and joining repair pathway may not be involved in thermo radiosensitization. We are now in the process of determining whether the homologous recombination (HR) repair pathway is involved in thermoradiosensitization using both hamster and chicken cell lines with knockouts in the HR repair pathway. In addition we are also exploring the role of nucleotide excision repair in thermo radiosensitization using XP cell lines. These results will be reported