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Cancer Cell. 2009 Jun 2;15(6):465-76. doi: 10.1016/j.ccr.2009.04.011.

Genetic p53 deficiency partially rescues the adrenocortical dysplasia phenotype at the expense of increased tumorigenesis.

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1
Department of Internal Medicine, University of Michigan Health System, Ann Arbor, MI 48109-2200, USA.

Abstract

Telomere dysfunction and shortening induce chromosomal instability and tumorigenesis. In this study, we analyze the adrenocortical dysplasia (acd) mouse, harboring a mutation in Tpp1/Acd. Additional loss of p53 dramatically rescues the acd phenotype in an organ-specific manner, including skin hyperpigmentation and adrenal morphology, but not germ cell atrophy. Survival to weaning age is significantly increased in Acd(acd/acd) p53(-/-) mice. On the contrary, p53(-/-) and p53(+/-) mice with the Acd(acd/acd) genotype show a decreased tumor-free survival, compared with Acd(+/+) mice. Tumors from Acd(acd/acd) p53(+/-) mice show a striking switch from the classic spectrum of p53(-/-) mice toward carcinomas. The acd mouse model provides further support for an in vivo role of telomere deprotection in tumorigenesis.

PMID:
19477426
PMCID:
PMC2703790
DOI:
10.1016/j.ccr.2009.04.011
[Indexed for MEDLINE]
Free PMC Article
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