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. 2008 Sep;180(1):601–609. doi: 10.1534/genetics.108.091967

TABLE 1.

Effect of p53 and genetic background on the development of neoplasms in ApcMin/+ mice

Extracolonic tumors
Intestinal tumor counta, mean ± SD (no. of mice)
Desmoid fibroma count, mean ± SD (no. of mice)
Pancreatic tumors, tumor bearing/totalb
B6 129 F1 B6 129 F1 B6 129 F1
Genotype Mom1R/Rc Mom1S/S Mom1R/S Mom1R/R Mom1S/S Mom1R/S Mom1S/S Mom1S/S Mom1R/S
ApcMin/+p53+/+ 27 ± 13 (13) 50 ± 50 (36) 62 ± 30 (27) 0 (8) 1 ± 2 (29) 3 ± 6 (19) 0/6 0/8 1/14
ApcMin/+p53+/BCM 40 ± 19 (28) 47 ± 26 (31) 84 ± 36 (77) 1 ± 2 (20) 2 ± 4 (24) 6 ± 5 (67) 0/13 0/2 0/49
ApcMin/+p53BCM/BCM 75 ± 25 (22) 46 ± 29 (10) 103 ± 36 (20) 33 ± 8 (22) 22 ± 4 (10) 28 ± 9 (17) 0/8c 9/9 8/9
Apc+/+p53BCM/BCM ND 0 (5) 0 (11) 0 (14) 0 (5) 0 (11) 0/6 0/3 0/11
a

Total tract.

b

Mice were scored as tumor bearing if a tumor was detected during necropsy at 90–100 days of age. Microscopic adenomas in the pancreas of some B6 ApcMin/+ p53tm1TyjJ/tm1TyjJ mice were detected only when the pancreas was sectioned and stained with hematoxylin and eosin.

c

Mom1 is a semidominant modifier of intestinal tumorigenesis that acts independently of p53 (Halberg et al. 2000). Testicular tumors were also observed in mice homozygous for p53BCM/BCM and heterozygous or homozygous for the 129 background, but not depending on Apc deficiency.