Dataset Information


Comparative genomic hybridization of mouse liver and tumors from Acd mutant and wild type strains in p53 deficient background

ABSTRACT: DNA from tumors of 10 male mice were competitively hybridized with DNA from liver samples from the same mouse on NimbleGen CGH arrays to assess copy number changes in the tumors. Four of the mice were wildtype for Acd (ortholog of human TPP1), 2 of which were p53-/- and 2 of which were p53-/+. The other 6 mice were homozygous for the mutant acd allele of Acd. 3 of these mice were p53-/- and the other 3 were p53-/+. Mice were crosses from double heterozygote parental mice. These parental mice were crosses of heterozygous Acd mutant mice (in a mixed DW/JxCAST/Ei background) with heterozygous null p53 mice (C57BL6/J; Trp53-tm1Tyj).

ORGANISM(S): Mus musculus  

TISSUE(S): Liver, Tumor

DISEASE(S): Tumor,Normal

SUBMITTER: Rork Kuick  

PROVIDER: E-TABM-680 | ArrayExpress | 2009-04-07


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

Else Tobias T   Trovato Alessia A   Kim Alex C AC   Wu Yipin Y   Ferguson David O DO   Kuick Rork D RD   Lucas Peter C PC   Hammer Gary D GD  

Cancer cell 20090601 6

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 Ac  ...[more]

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