It is generally recognized that rodent models for analysis and prevention of carcinogenesis
can be classified into three categories, i.e., traditional chemical carcinogenic,
chronic inflammatory, and transgenic or gene-knockout animal models. With our knowledges
about basic mechanisms and etiology of human carcinogenesis, the transfer
from traditional chemical carcinogenesis models to chronic inflammation or genetic
model is now in fashion. Although the primary objective of the model developments is
to elucidate the basic mechanism and etiology of carcinogenesis, those models are
being adapted into chemoprevention studies and used for identifying potential
chemopreventive agents. Mouse lines that harbor germ-line mutation in Apc gene
such as ApcMin/+, Apc Δ716, Apc Δ474 and so forth are being considered to be useful animal
models for investigating colorectal cancer chemopreventive agents because they bear
similarities in molecular and genetic mechanisms to humans and, therefore,
spontaneously develop numerous polyps in intestines, as in human familial
adenomatous polyposis coli, and require relatively short period (12～15 weeks) to
develop grossly identifiable tumors. Even though the relevance or extrapolation of data
from gene-mutated mice remains to be validated further, Apc gene-mutated mice
model in practice would be more applicable in chemoprevention studies than any other
gene-mutated models.

Keywords: Apc, Carcinogenesis, Chemoprevention, Gene-mutated animal model