Open AccessMultistep carcinogenesis of the colon in Apc Min/+ mouse
Author(s) -
Yamada Yasuhiro,
Mori Hideki
Publication year - 2007
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2006.00348.x
Subject(s) - carcinogenesis , epigenetics , adenomatous polyposis coli , colorectal cancer , mutant , familial adenomatous polyposis , cancer research , biology , mutation , gene , microbiology and biotechnology , pathology , cancer , genetics , medicine
Colon cancer arises through different histological stages representing different genetic and epigenetic alterations. The Apc Min/+ mouse has a point mutation at the Apc gene, and it is considered to be a model for human familial adenomatous polyposis. Our previous studies have revealed the presence of a number of intramucosal microadenomas in the colons of Apc Min/+ mice, in which only a few macroscopic tumors were recognized. These observations suggest that there are two distinct stages for colon carcinogenesis in Apc Min/+ mouse, and the Apc Min/+ mouse is regarded as a good model to study multistage colon carcinogenesis. A number of genes that modify intestinal tumorigenesis have been identified using Apc mutant mice combined with other mutant mice. It has become apparent that epigenetic modification strongly affects intestinal tumorigenesis in Apc Min/+ mice. We herein describe the different stages of colon tumorigenesis and their modifiers, and discuss the possible application of Apc mutant mice in order to better understand the molecular mechanisms of multistage carcinogenesis in the large bowel of humans. ( Cancer Sci 2007; 98: 6–10)