Brian Lehmann
Last active: 9/15/2015

Radiosensitization of prostate cancer by priming the wild-type p53-dependent cellular senescence pathway.

Lehmann BD, McCubrey JA, Terrian DM
Cancer Biol Ther. 2007 6 (8): 1165-70

PMID: 18059157 · PMCID: PMC2889025 · DOI:10.4161/cbt.6.8.4544

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.

MeSH Terms (10)

Apoptosis Cell Line, Tumor Cellular Senescence DNA Damage Humans Male Models, Biological Prostatic Neoplasms Signal Transduction Tumor Suppressor Protein p53

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