DNA mismatch repair and low dose hyper-radiosensitivity in prostate cancer cells

Abstract

Low-dose hyper-radiosensitivity (HRS) describes the excessive sensitivity of cells to radiation doses less than 0.3Gy. Evidence suggests that HRS may influence tumour response and normal tissue reactions after intensity modulated radiotherapy and low dose rate brachytherapy, and that the response may potentially be exploited to improve therapeutic efficacy. Prostate cancer (PCa) is particularly likely to be affected by HRS due to the increasing use of protocols that involve low doses of radiation or low dose rates used in the radiotherapeutic management of the disease. While accumulating evidence indicates that DNA repair and G2 checkpoint responses are involved in the manifestation of HRS, the underlying mechanism(s) remains unknown. Elucidation of the mechanism(s) of the response is fundamental to understanding the true implications of HRS for radiotherapy practice.