The Min mouse, generated by random germline mutagenesis, carries a mut
ation in the mouse homolog of APC and is a model of inherited human in
testinal tumorigenesis. To identify other genes in the pathway(s) of i
ntestinal tumorigenesis, genes that modify the Min phenotype have been
sought. Several have been identified, including Mom1 and the genes fa
r the 5-cytosine DNA methyltransferase and the DNA mismatch repair fac
tor Msh2. Min-dependent tumorigenesis also occurs in mammary glands, t
he pancreas, and the body wall. The Min mouse has therefore became a m
odel for tumorigenesis in a variety of organs. Identifying modifiers o
f its phenotype will help in piecing together the pathways of tumorige
nesis in each of these tissues.