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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Spontaneous and carcinogen-induced tumorigenesis in p53-deficient mice.

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.[1]

References

  1. Spontaneous and carcinogen-induced tumorigenesis in p53-deficient mice. Harvey, M., McArthur, M.J., Montgomery, C.A., Butel, J.S., Bradley, A., Donehower, L.A. Nat. Genet. (1993) [Pubmed]
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