02087nas a2200241 4500008004100000245009200041210006900133260000900202300001100211490000600222520128500228653001201513653002101525653002701546653001101573653001501584653000901599653001901608653002101627100002501648700001801673856015401691 2002 eng d00aKnockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer?0 aKnockout and transgenic mice of Trp53 what have we learned about c2002 a101-110 v43 a
The human p53 tumor suppressor gene TP53 is mutated at a high frequency in sporadic breast cancer, and Li-Fraumeni syndrome patients who carry germline mutations in one TP53 allele have a high incidence of breast cancer. In the 10 years since the first knockout of the mouse p53 tumor suppressor gene (designated Trp53) was published, much has been learned about the contribution of p53 to biology and tumor suppression in the breast through the use of p53 transgenic and knockout mice. The original mice deficient in p53 showed no mammary gland phenotype. However, studies using BALB/c-Trp53-deficient mice have demonstrated a delayed involution phenotype and a mammary tumor phenotype. Together with other studies of mutant p53 transgenes and p53 bitransgenics, a greater understanding has been gained of the role of p53 in involution, of the regulation of p53 activity by hormones, of the effect of mouse strain and modifier genes on tumor phenotype, and of the cooperation between p53 and other oncogenic pathways, chemical carcinogens and hormonal stimulation in mammary tumorigenesis. Both p53 transgenic and knockout mice are important in vivo tools for understanding breast cancer, and are yet to be exploited for developing therapeutic strategies in breast cancer.
10aAnimals10aBreast Neoplasms10aDisease Models, Animal10aFemale10aGenes, p5310aMice10aMice, Knockout10aMice, Transgenic1 aBlackburn, Anneke, C1 aJerry, Joseph uhttps://www.umass.edu/veterinary-animal-sciences/research-faculty/publications/knockout-and-transgenic-mice-of-trp53-what-have-we-learned-about-p53-0