Genetic background alters the spectrum of tumors that develop in p53-deficient mice - PubMed (original) (raw)
Genetic background alters the spectrum of tumors that develop in p53-deficient mice
M Harvey et al. FASEB J. 1993 Jul.
Abstract
Using gene targeting in embryonic stem cells, we have generated mice with one or two null p53 germ line alleles. Mice with both p53 alleles inactivated are developmentally normal but highly susceptible to the early development of spontaneous tumors. Initial studies were performed in mice with a mixed inbred genetic background (75% C57BL/6 and 25% 129/Sv) (Donehower et al., Nature (London) 356, 215-221, 1992). To study the effect of genetic background on tumorigenesis in p53-deficient mice, we have put the p53 null allele into a pure 129/Sv background and monitored tumor development. 129/Sv mice with two p53 null alleles developed tumors sooner than the mixed genetic background p53-deficient animals. The most frequently observed tumor in p53 null mice of both genetic backgrounds was a malignant lymphoma. Because the 129/Sv strain has a low incidence of lymphoma, the frequent occurrence of lymphomas in all p53 null mice suggests that this particular tumor type may be a direct result of p53 loss and not a result of a particular genetic background. In addition to malignant lymphomas, the 129/Sv p53-deficient mice showed an increased incidence of aggressive teratocarcinomas (8 of 18 tumor-bearing males), a tumor type rare in virtually all inbred mice except for 129 strains. Thus, it appears that loss of p53 may accelerate a prior tumor predisposition and that genetic background can play a role in mediating both the rate and spectrum of tumor development in these mice.
Similar articles
- Effects of genetic background on tumorigenesis in p53-deficient mice.
Donehower LA, Harvey M, Vogel H, McArthur MJ, Montgomery CA Jr, Park SH, Thompson T, Ford RJ, Bradley A. Donehower LA, et al. Mol Carcinog. 1995 Sep;14(1):16-22. doi: 10.1002/mc.2940140105. Mol Carcinog. 1995. PMID: 7546219 - Spontaneous and carcinogen-induced tumorigenesis in p53-deficient mice.
Harvey M, McArthur MJ, Montgomery CA Jr, Butel JS, Bradley A, Donehower LA. Harvey M, et al. Nat Genet. 1993 Nov;5(3):225-9. doi: 10.1038/ng1193-225. Nat Genet. 1993. PMID: 8275085 - Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours.
Donehower LA, Harvey M, Slagle BL, McArthur MJ, Montgomery CA Jr, Butel JS, Bradley A. Donehower LA, et al. Nature. 1992 Mar 19;356(6366):215-21. doi: 10.1038/356215a0. Nature. 1992. PMID: 1552940 - The p53-deficient mouse: a model for basic and applied cancer studies.
Donehower LA. Donehower LA. Semin Cancer Biol. 1996 Oct;7(5):269-78. doi: 10.1006/scbi.1996.0035. Semin Cancer Biol. 1996. PMID: 9110404 Review. - Is p53 haploinsufficient for tumor suppression? Implications for the p53+/- mouse model in carcinogenicity testing.
Venkatachalam S, Tyner SD, Pickering CR, Boley S, Recio L, French JE, Donehower LA. Venkatachalam S, et al. Toxicol Pathol. 2001;29 Suppl:147-54. doi: 10.1080/019262301753178555. Toxicol Pathol. 2001. PMID: 11695551 Review.
Cited by
- The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability.
Abad E, Sandoz J, Romero G, Zadra I, Urgel-Solas J, Borredat P, Kourtis S, Ortet L, Martínez CM, Weghorn D, Sdelci S, Janic A. Abad E, et al. J Exp Clin Cancer Res. 2024 Apr 29;43(1):127. doi: 10.1186/s13046-024-03045-4. J Exp Clin Cancer Res. 2024. PMID: 38685100 Free PMC article. - The complete Kaposi sarcoma-associated herpesvirus genome induces early-onset, metastatic angiosarcoma in transgenic mice.
Sin SH, Eason AB, Kim Y, Schneider JW, Damania B, Dittmer DP. Sin SH, et al. Cell Host Microbe. 2024 May 8;32(5):755-767.e4. doi: 10.1016/j.chom.2024.03.012. Epub 2024 Apr 22. Cell Host Microbe. 2024. PMID: 38653242 - Arsenic trioxide extends survival of Li-Fraumeni syndrome mimicking mouse.
Li J, Xiao S, Shi F, Song H, Wu J, Zheng D, Chen X, Tan K, Lu M. Li J, et al. Cell Death Dis. 2023 Nov 29;14(11):783. doi: 10.1038/s41419-023-06281-2. Cell Death Dis. 2023. PMID: 38030599 Free PMC article. - Protein-level mutant p53 reporters identify druggable rare precancerous clones in noncancerous tissues.
Yao P, Xiao P, Huang Z, Tang M, Tang X, Yang G, Zhang Q, Li X, Yang Z, Xie C, Gong H, Wang G, Liu Y, Wang X, Li H, Jia D, Dai L, Chen L, Chen C, Liu Y, Xiao H, Zhang Y, Wang Y. Yao P, et al. Nat Cancer. 2023 Aug;4(8):1176-1192. doi: 10.1038/s43018-023-00608-w. Epub 2023 Aug 3. Nat Cancer. 2023. PMID: 37537298 - Disruption of tp53 leads to cutaneous nevus and melanoma formation in Xenopus tropicalis.
Ran R, Li L, Shi Z, Liu G, Jiang H, Fang L, Xu T, Huang J, Chen W, Chen Y. Ran R, et al. Mol Oncol. 2022 Oct;16(19):3554-3567. doi: 10.1002/1878-0261.13301. Epub 2022 Aug 18. Mol Oncol. 2022. PMID: 35981147 Free PMC article.
Publication types
MeSH terms
LinkOut - more resources
Full Text Sources
Other Literature Sources
Molecular Biology Databases
Research Materials
Miscellaneous