| First Author | Teraoka N | Year | 2011 |
| Journal | Int J Cancer | Volume | 129 |
| Issue | 3 | Pages | 528-35 |
| PubMed ID | 20886595 | Mgi Jnum | J:173807 |
| Mgi Id | MGI:5050381 | Doi | 10.1002/ijc.25711 |
| Citation | Teraoka N, et al. (2011) High susceptibility to azoxymethane-induced colorectal carcinogenesis in obese KK-Ay mice. Int J Cancer 129(3):528-35 |
| abstractText | Obesity is associated with colon carcinogenesis. However, not much information is available regarding the mechanisms of obesity-associated colorectal cancer, and there are only few useful animal models for investigating the underlying mechanism between obesity and colorectal cancer. KK-A(y) mice exhibit severe obesity. Amount of visceral fat assessed by micro-computed tomography was almost 15 times higher than that of same aged C57BL/6J mice. Treatment with azoxymethane (AOM; 200 mug/mouse injected once a week for 3 times) resulted in markedly increased colon aberrant crypt foci (ACF) development ( approximately 70 ACF/mouse) in KK-A(y) mice compared with lean C57BL/6J mice ( approximately 9 ACF/mouse). Moreover, administration of AOM at a dose of 200 mug/mouse once a week for 6 times developed colorectal adenocarcinomas within only 7 weeks after the last AOM injection. The incidence of adenocarcinoma was 88% in KK-A(y) mice and was markedly higher than the 4% observed in C57BL/6J mice. The number of tumors/mouse was 7.80 in KK-A(y) mice and also markedly higher than the 0.12 in the C57BL/6J case. Interestingly, adenocarcinomas were observed in most of the AOM-treated KK-A(y) mice along with remarkable tumor angiogenesis, and some showed submucosal invasion. These results indicate that the KK-A(y) mouse, featuring intact leptin and leptin receptor Ob-Rbl, could be a useful animal model to investigate obesity-associated cancer. |
