Abstract
Chromosomal abnormalities have been assessed in 153-deficient mice. The in vivo frequency of spontaneous stable aberrations in bone marrow cells was elevated by approximately 20-fold in p53 nulls and 13-fold in p53 heterozygotes compared to wild-type. No excessive induction of stable aberrations by y-irradiation was observed, but p53 deficiency resulted in excess radiation-induced hyperploidy (>10-fold wild-type frequency). No influence of pS3 genotype on sister chromatid exchange or G2 chromatid damage was observed in mitogen-stimulated spleen cell cultures; however, a p53 effect on postirradiation mitotic entry was seen. Abnormalities in chromosome segregation and mitotic delay following irradiation in p53-deficient mice suggest a G2-M checkpoint role for p53 and are broadly consistent with data on tumorigenesis in these animals.
Original language | English |
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Pages (from-to) | 3883-3889 |
Number of pages | 7 |
Journal | Cancer Research |
Volume | 55 |
Issue number | 17 |
Publication status | Published - 1 Sept 1995 |