Abstract
Thermal radiosensitization was tested in a pair of mouse cells (MB+ wild-type and MB−, DNA polymerase β knockout cells) and in human breast carcinoma cells (MCF7 wild-type and C716 transfected to give elevated DNA polymerase β expression). Results showed that neither reducing DNA polymerase β (involved in base excision repair) nor increasing it had any significant effect on thermal radiosensitization. The data indicated that polymerase β was not involved in thermal radiosensitization, and since hyperthermia is known as a radiation damage repair inhibitor, other repair pathways might be involved and need to be explored.