DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice
J. Clin. Invest. Lisiane B. Meira, et al. 118:2516 doi:10.1172/JCI35073 [Go to this article.]

Figure 5
Induction of εA, εC, and 8oxoG lesions by chronic inflammation and Ctnnb1 mutations in colon tumors. Six- to 8-week-old male mice were untreated or were administered 2.5% DSS for 5 days and euthanized 1 or 7 days after treatment. Levels of the modified bases εA (A), εC (B), and 8oxoG (C) were measured from colonic mucosal DNA and are shown for Aag-proficient (+) and Aag-deficient (–) mice. Within treatment groups, we observed no differences between Aag^+/+ and Aag^–/– mice, and thus these genotypes were combined in the analysis. Data are mean ± SD. (D–F) Point mutations in Ctnnb1. (D and E) Chromatogram showing an example of the most common mutation observed, a G:C to A:T transition in codon 41 of Ctnnb1. The arrow indicates the peaks for the mutant and WT sequences. (E and F) Distribution of mutations in Ctnnb1. Base substitutions are indicated below the sequence, and their frequencies are shown for the different experimental groups. (F) Deletion mutants in Ctnnb1. Chromatograms of the 2 deletion mutants are shown with an arrow below the sequence indicating the deletion junction. Also shown is the deleted sequence (lowercase) with red highlighting of regions of microhomology between the deleted portion and the adjacent retained sequence.