p53-deficient mice are extremely susceptible to radiation-induced tumorigenesis.
Mice constitutively lacking alleles of the p53 tumour suppressor gene spontaneously develop lymphomas and sarcomas. We report here that a single dose of 4 Gy radiation dramatically decreases the latency for tumour development in p53 heterozygous mice. The pattern of genetic alterations at the remaining wild type allele in these tumours differs substantially from spontaneous tumours from similar mice indicating that p53 itself may have been a target for radiation-induced alterations. Lower dose irradiation (1 Gy) of preweanling p53 null mice also significantly decreases tumour latency, suggesting that there are additional genetic targets involved in radiation-induced malignancy. Thus p53-deficient mice provide a sensitive model system for studies of the consequences of radiation exposure.
Kemp
C J
CJ
CRC Beatson Laboratories, Beatson Institute for Cancer Research, Bearsden, Glasgow, UK.
Wheldon
T
T
Balmain
A
A
D000818:Animals; D016158:Genes, p53; D006579:Heterozygote; D008223:Lymphoma / Q000235:genetics*; D051379:Mice; D008954:Models, Biological; D009154:Mutation; D009381:Neoplasms, Radiation-Induced / Q000235:genetics*; D012513:Sarcoma, Experimental / Q000235:genetics*; D013997:Time Factors