Pg 1 staining showing PAPG. and Kinzler,K.W. While there was no significant difference between (+/+) and (+/−) gastric tumor incidences in both middle term and long term experiments (experiments II and III) for males and females, the reduction in p53 gene dosage was associated with earlier mortality due to induced lymphomas and sarcomas. Vogelstein,B. MNU (Sigma, St Louis, MO) was dissolved in distilled water and freshly prepared three times per week. MNU or water as a control. Sci Rep. 2020 Oct 5;10(1):16514. doi: 10.1038/s41598-020-73463-9. Matching numbers of each mouse genotype were given distilled water for the same period as controls. p53 (−/−) mice survived less with (aP<0.001) or without (bP<0.05) MNU treatment but the latter showed a higher death rate (cP<0.05). In experiment III, MNU up to 120 p.p.m. Any mice in which gene activity is altered by manipulation of DNA sequence is called transgenic mice: that includes knockout, sequence insertion or deletion Cite 30th Dec, 2015 Thus while survival was impaired to the extent that homozygous KO mice could not be included in the long term study, a clear conclusion of enhanced susceptibility was possible. A detailed explanation of how knockout (KO) mice are created is located at the website of the Nobel Prize in Physiology or Medicine 2007. Survival curves of mice treated with MNU in experiment III. USA.gov. and Sugimura,Y. Five-week-old wild-type (+/+), heterozygous (+/–) and nullizygous (–/–) p53 KO mice were used in experiments I and II. Despite these potential limitations, p53 KO mice provide a powerful tool for short term carcinogenicity studies. Exp, experiment; S, death. (, Tatematsu,M., Mutai,M., Aoki,T., de Camargo,J.L., Furihata,C. These results suggest that p53 may not be a direct target of MNU but rather play an important role as a gatekeeper in mouse stomach carcinogenesis induced by this direct acting agent. (, Greenblatt,M.S., Bennett,W.P., Hollstein,M. 1997 Oct 31;278(5339):803-4. doi: 10.1126/science.278.5339.803. Although chronically anemic, most animals survived for 2 to 9 months and were fertile. Macrophage metabolic adaptation to heme detoxification involves CO-dependent activation of the pentose phosphate pathway. Hundreds of these oncomice have been developed covering a wide range of cancers affecting most organs of the body and they are being refined to become more representative of human cancer. Masami Yamamoto, Tetsuya Tsukamoto, Hiroki Sakai, Norimitsu Shirai, Hiroko Ohgaki, Chie Furihata, Lawrence A. Donehower, Kenji Yoshida, Masae Tatematsu, p53 knockout mice (–/–) are more susceptible than (+/–) or (+/+) mice to N-methyl-N-nitrosourea stomach carcinogenesis, Carcinogenesis, Volume 21, Issue 10, 1 October 2000, Pages 1891–1897, https://doi.org/10.1093/carcin/21.10.1891. A second generation transgenic mouse model expressing both hemoglobin S (HbS) and HbS-Antilles results in increased phenotypic severity. and Ito,N. (. and Ito,N. There are several thousand different strains of knockout mice. NIH and Matsushima,T. Sequencing was performed using an AmpliCycle Sequencing Kit (Perkin Elmer) as described previously (28). Consideration must also be given to the genetic background of the mouse strain and the impact of strain variability on disease and toxicity models. MNU there was no significant difference in the incidence of gastric tumors between p53 (+/+) and (+/–) mice. Kemp et al. The embryonic stem cells that incorporated the knocked-out gene are isolated from the unaltered cells using the marker gene from step 1. PCR primers for genotyping and for SSCP analysis of mouse p53 analysis, Incidence of gastric lesions at experimental week 15, Incidence of gastric tumors at experimental week 40. The experimental design is shown in Figure 1. However, complete loss of wild-type p53 expression greatly enhanced stomach carcinogenesis. Transgenic mouse models from Charles River provide researchers with high-quality, validated research models for gene research and drug development. Experimental design. Curr Opin Hematol. and Takahashi,M. 2020 May;40(5):1220-1230. doi: 10.1161/ATVBAHA.120.314045. and Donehower,L.A. Int J Mol Sci.

and Nakanishi,H. For full access to this pdf, sign in to an existing account, or purchase an annual subscription.

(, Furihata,C., Tatematsu,M., Saito,M., Ishida,S., Nakanishi,H., Inada,K., Tei,H., Hattori,M., Ito,T. In the control groups, the frequencies were 4.1 ± 2.1, 5.0 ± 0.4 and 6.2 ± 3.2 in p53 (+/+), (+/−) and (−/−) mice, respectively. (, Furihata,C., Saito,D., Fujiki,H., Kanai,Y., Matsushima,T. Four pairs of PCR primers for mouse p53 exons 5–8 were designed based on the published sequences (27) as listed in Table I. PCR was performed with a Takara PCR Thermal Cycler MP and products electrophoresed in 0.625× MDE polyacrylamide gels (FMC, Rockland, ME) with 5% glycerol. (, Shimokado,K., Watanabe,H., Sumii,M., Miyagawa,K., Kamiya,K., Dohi,K. (, Furihata,C., Iwasaki,Y., Sugimura,T., Tatematu,M. Transgenic mouse models of sickle cell disease. These tumors were not epithelial in origin but usually lymphomas and sarcomas. and Nomura,T.

(, Tatematsu,M., Saito,D., Furihata,C., Miyata,Y., Nakatsuka,T., Ito,N. Random vs. The functions of the p53 protein include a contribution to G1 cell cycle arrest to allow DNA repair as well as induction of apoptosis after DNA damage (8).

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