Spontaneous and carcinogen-induced tumorigenesis in p53-deficient mice - PubMed (original) (raw)
Spontaneous and carcinogen-induced tumorigenesis in p53-deficient mice
M Harvey et al. Nat Genet. 1993 Nov.
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.
Comment in
- Experimental models of human carcinogenesis.
Kastan MB. Kastan MB. Nat Genet. 1993 Nov;5(3):207-8. doi: 10.1038/ng1193-207. Nat Genet. 1993. PMID: 8275078 No abstract available.
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