NDLI: High metastatic potential in mice inheriting a targeted p53 missense mutation

Content Provider	PubMed Central
Author	Liu, Geng Mcdonnell, Timothy J. Luna, Roberto Montes De Oca Kapoor, Mini Mims, Betsy El-naggar, Adel K. Lozano, Guillermina
Copyright Year	2000
Abstract	To understand the relevance of p53 missense mutations in vivo, we generated a mouse containing an arg-to-his substitution at p53 amino acid 172, which corresponds to the R175H hot-spot mutation in human tumors by homologous recombination. Inadvertently, this mouse contains the additional deletion of a G nucleotide at a splice junction that attenuates levels of mutant p53 to near wild-type levels. Mice heterozygous for the mutant allele differed from p53 +/− mice in tumor spectrum, with a significant increase in the number of carcinomas and a slight decrease in the number of lymphomas. More importantly, the osteosarcomas and carcinomas that developed in these mutant mice frequently metastasized (69% and 40%, respectively). In contrast, metastasis is rare in osteosarcomas of p53 +/− mice. Loss of heterozygosity studies of tumors indicated loss of heterozygosity in only 1 of 11 tumors. These data indicate clear differences between a p53 missense mutation and a null allele in tumorigenesis in vivo and suggest that the p53R172HΔg mutant represents a gain-of-function allele.
Starting Page	4174
File Format	PDF
ISSN	10916490
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	8
Volume Number	97
Language	English
Publisher	The National Academy of Sciences
Publisher Date	2000-04-11
Access Restriction	Open
Rights Holder	The National Academy of Sciences
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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High metastatic potential in mice inheriting a targeted p53 missense mutation.

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