International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


Mr. Kevin Haigis
University of Wisconsin - Madison
McArdle Laboratory for Cancer Research
1400 University Avenue
Madison, WI 53706

Co-Authors: Dove W.F.
Institutions: University of Wisconsin Madison, McArdle Laboratory for Cancer Research

Apc<Min/+> (Min/+) mice carry a truncating mutation at codon 850 of Apc and develop multiple intestinal neoplasms. Somatic loss of function of the wild type allele of Apc is required for intestinal tumorigenesis in Min mice. Nevertheless, the mechanism by which this somatic event occurs is regulated by genetic background. Min represents a powerful tool with which to study the genetic pathways important in intestinal tumorigenesis, both upstream and downstream of the pivotal loss of Apc function. On the C57BL/6 (B6) genetic background, loss of Apc function in intestinal adenomas occurs exclusively by loss of heterozygosity (LOH). Using interphase fluorescent in situ hybridization (FISH), we have found that adenomas from B6 Min/+ mice are disomic for the Apc chromosome, 18, and that the Apc locus is homozygous for the Min allele. Through molecular and cytogenetic analysis, we find no evidence for genomic instability in tumors from Min/+ mice. Further, in experiments utilizing the Robertsonian translocation Rb(7.18)9Lub (Rb9), we have found that the LOH event in B6 Min/+ mice occurs by mitotic recombination. We also find that Rb9 acts as a semi-dominant suppressor of tumor multiplicity, while exerting no effect on the size or regional distribution of tumors from Min/+ mice. Thus, modifiers of the Min phenotype need not be polymorphic at the level of chromosome structure.

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