Abstract
Using gene targeting techniques, mice that have been generated with two germ–line p53 null alleles (homozygotes) develop normally but are highly susceptible to early onset spontaneous tumours. Here, we show that mice with a single null p53 allele (heterozygotes) produced in the same way are also susceptible to spontaneous tumours, but with a delayed onset compared to homozygotes. The most frequent tumour type in homozygotes was malignant lymphoma; in heterozygotes, osteosarcomas and soft tissue sarcomas predominated. Heterozygous mice treated with a liver carcinogen, dimethylnitrosamine, showed a decreased survival time in comparison to treated wild type mice, suggesting that the p53–deficient mice may be useful for some in vivo carcinogenesis assays.
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Harvey, M., McArthur, M., Montgomery, C. et al. Spontaneous and carcinogen–induced tumorigenesis in p53–deficient mice. Nat Genet 5, 225–229 (1993). https://doi.org/10.1038/ng1193-225
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DOI: https://doi.org/10.1038/ng1193-225
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