Role of p53 mutations in the radiosensitivity status of tumor cells

Wild-type p53 is involved in cellular response to DNA damage including cell cycle control, DNA repair and activation of apoptosis, Accumulation of p53 protein following DNA damage may initiate the apoptotic process, resulting rn cell death. DNA damage induced by radiation is an example of apoptotic stimulus involving p53, Regulation of apoptosis by p53 can occur through tr anscriptional regulation of pro-apoptotic (e.g. bar) and anti-apoptotic (e. g. bel-2) factors. Although wild-type p53 usually sensitizes cells to radia tion therapy, p53 mutations have a variable effect on radiation response. F or example p53 mutations in bone or breast tumors have been found to be ass ociated with resistance to chemotherapeutic drugs or ionizing radiation, Mu tated p53 has has been reported to increase sensitivity to radiation and dr ugs in colorectal and bladder tumors, The present brief commentary tries to find an explanation at molecular level of these conflicting results.