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Department of Microbiology and Immunology, Kimmel Cancer Center, Jefferson Medical College, Philadelphia, Pennsylvania 19107 [R. K., L. D. S.], and Biostatistics Section, Department of Medicine, Jefferson Medical College, Philadelphia, Pennsylvania 19107 [E. P., W. W. H.]
Intestinal adenoma development in ApcMin mice is influenced by genetic background. We generated a congenic line between the CAST and B6 inbred strains to study the effects of a resistant CAST background in the absence of a major modifier locus, Modifier of Min 1 (Mom1R). Progeny from a CAST.B6 Mom1R/S x B6 ApcMin/+ intercross were 110 or 200 days of age and screened for intestinal polyps. There was a significant decrease (P < 0.0001) in polyp multiplicity and size in CASTB6F1 Mom1R/S, ApcMin/+ and CASTB6F1 Mom1S/S, ApcMin/+ progeny compared with B6 Mom1S/S, ApcMin/+ controls. A complete absence of colon polyps was observed in all mice heterozygous for the CAST background. These results demonstrate that the CAST strain carries dominant modifier loci, in addition to Mom1R, that dramatically reduce polyp burden in the small intestine and eliminate polyp burden in the colon of ApcMin mice.
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A. A. Baran, K. A. Silverman, J. Zeskand, R. Koratkar, A. Palmer, K. McCullen, W. J. Curran Jr, T. B. Edmonston, L. D. Siracusa, and A. M. Buchberg The modifier of Min 2 (Mom2) locus: Embryonic lethality of a mutation in the Atp5a1 gene suggests a novel mechanism of polyp suppression Genome Res., May 1, 2007; 17(5): 566 - 576. [Abstract] [Full Text] [PDF] |
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