| First Author | Yan B | Year | 2009 |
| Journal | Carcinogenesis | Volume | 30 |
| Issue | 10 | Pages | 1776-80 |
| PubMed ID | 19541853 | Mgi Jnum | J:153451 |
| Mgi Id | MGI:4365490 | Doi | 10.1093/carcin/bgp146 |
| Citation | Yan B, et al. (2009) Increased skin carcinogenesis in caspase-activated DNase knockout mice. Carcinogenesis 30(10):1776-80 |
| abstractText | Caspase-activated DNase (CAD), also called DNA fragmentation factor (DFF), is the enzyme responsible for DNA fragmentation during apoptosis, a hallmark of programmed cell death. CAD/DFF has been shown to suppress radiation-induced carcinogenesis by preventing genomic instability in cells. In this study, we have investigated the role of CAD in chemical carcinogenesis using CAD-null mice and two-stage model of skin carcinogenesis. After topical treatment of mouse skin with dimethylbenz[a]anthracene (DMBA) as an initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as a promoting agent, there was a 4-fold increase in the number of papillomas per mouse and 50.8% increase in the incidence of papilloma formation in the CAD knockout mice compared with wild-type littermates. The papillomas in CAD-null mice grew faster and reached larger sizes. These data indicate that loss of CAD function enhances tumorigenesis induced by a chemical carcinogen in the DMBA/TPA two-stage model of skin carcinogenesis in mice. |
