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lüll Radiosensitization of prostate cancer by priming the wild-type p53-dependent cellular senescence pathway Lehmann BD; McCubrey JA; Terrian DMCancer Biol Ther 2007[Aug]; 6 (8): 1165-70A dramatic stage-migration in diagnosis of prostate cancer has led to earlier detection of clinically localized carcinoma and an increased use of radiation therapy. The p53 protein responds to irradiation-induced DNA damage by removing critically damaged cells from the proliferative pool. This review will focus on the dominant role that p53-dependent cellular senescence, rather than cell death, plays in determining the radiosensitivity of human prostate cancer cells in vitro. The finding that senescence is a primary mechanism of tumor regression indicates that p53 activators or downstream effectors may prove effective in radiosensitizing some carcinoma of the prostate.|Apoptosis/physiology/radiation effects[MESH]|Cell Line, Tumor[MESH]|Cellular Senescence/physiology/*radiation effects[MESH]|DNA Damage[MESH]|Humans[MESH]|Male[MESH]|Models, Biological[MESH]|Prostatic Neoplasms/pathology/physiopathology/*radiotherapy[MESH]|Signal Transduction/physiology/*radiation effects[MESH]|Tumor Suppressor Protein p53/*physiology[MESH] |