Journal Article

Increased skin carcinogenesis in caspase-activated DNase knockout mice

Bin Yan, Huili Wang, Donghua Xie, Nobuko Wakamatsu, Mitchell S. Anscher, Mark W. Dewhirst, Ron E.J. Mitchel, Benny J. Chen and Chuan-Yuan Li

in Carcinogenesis

Volume 30, issue 10, pages 1776-1780
Published in print October 2009 | ISSN: 0143-3334
Published online June 2009 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgp146
Increased skin carcinogenesis in caspase-activated DNase knockout mice

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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.

Journal Article.  2913 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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