Radiosensitization of prostate cancer by priming the wild-type p53-dependent cellular senescence pathway.
A 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.
Departments of Anatomy and Cell Biology, Brody School of Medicine at East Carolina University, Greenville, North Carolina, USA.
Brian D
BD
Lehmann
James A
JA
McCubrey
David M
DM
Terrian
D017209:Apoptosis / Q000502:physiology / Q000528:radiation effects; D045744:Cell Line, Tumor; D016922:Cellular Senescence / Q000502:physiology / Q000528:radiation effects*; D004249:DNA Damage; D006801:Humans; D008297:Male; D008954:Models, Biological; D011471:Prostatic Neoplasms / Q000473:pathology / Q000503:physiopathology / Q000532:radiotherapy*; D015398:Signal Transduction / Q000502:physiology / Q000528:radiation effects*; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*
D016159:Tumor Suppressor Protein p53