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.
Lehmann
Brian D
BD
Departments of Anatomy and Cell Biology, Brody School of Medicine at East Carolina University, Greenville, North Carolina, USA.
McCubrey
James A
JA
Terrian
David M
DM
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