Susceptibility to radiation-carcinogenesis and accumulation of chromosomal breakage in p53 deficient mice.

摘要: The p53 tumour suppressor gene is an important participant in the cellular response to ionizing radiation and other DNA damaging agents. Cells which lack are unable arrest cell cycle or enter into apoptotic death following irradiation. Moreover, these deficient cells exhibit increased resistance agents, including radiation. significance of this radiation-resistance its relationship role that plays suppression has not yet been determined. In report we have analyzed mice, expressing either a mutant transgene having targeted null allele, order investigate governing susceptibility radiation-carcinogenesis controlling vivo accumulation chromosomal abnormalities. We show wild-type critical gamma-radiation-induced tumorigenesis, sarcomas lymphomas rapidly appear irradiated transgenic mice. associated with two-fold increase radiation-induced double stranded breaks relative observed animal. Taken together, observations suggest acts suppress formation by preventing sustained damage.