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K-RasLA2 mice develop early-onset lung adenocarcinomas [22].
It has been reported previously that C57BL mice develop early-onset osteoarthritis when fed a high-fat diet [ 26].
Despite the low expression levels of mutant APP, Tg-SwDI mice develop early-onset robust accumulation of Aβ in the brain.
In contrast to Irs-1-/ mice, Irs-2-deficient mice develop early-onset diabetes due to a combination of peripheral insulin resistance and a loss of β-cell function [ 13, 15].
When R26PR is mated to either of two Cre lines, Mx1-cre or MMTV-cre, mice develop early-onset T-cell acute lymphoblastic leukemia (T-ALL) with median overall survival of 41 and 64 days for R26PR Mx1-cre and R26PR Mx1-cree, respectively.
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After 10 weeks of treatment with 0.01% BBN, the mice developed early-onset muscle-invasive UCC in 50% of cases, compared with 0% in mice carrying either mutation alone.
Cngb3−/− mice develop early onset, slow progression of cone degeneration (30).
The female SKG mice developed earlier onset and more severe arthritis compared with males (Fig. 1b, c), further confirming the sex × gene interaction in the disease phenotype of SKG mice [ 16, 29].
Unlike p53 null mice, which rapidly succumb to lymphomas, p53 3KR/3KR) mice did not develop early-onset lymphomas.
Heterozygous Msh2, Msh6, and Mlh1 knockout mice do not develop early-onset tumors, but homozygous Msh2, Msh6, and Mlh1 knockout mice are cancer-prone, developing tumors in multiple organs including the gastrointestinal tract.
Although the p53 target gene p21 CDKN1A is critical for inducing p53-dependent senescence and cell-cycle arrest, mice lacking p21 are not prone to develop early-onset tumors (Choudhury et al., 2007).
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