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 3
Increased severity of disease in Aag–/– versus Aag+/+ animals treated with 7 cycles of DSS. (A) Treatment scheme. (B) Decrease in colon length for Aag–/– animals (n = 18) compared with Aag+/+ animals (n = 7). (C) Increase in spleen weight as a percentage of body weight for Aag+/+ (n = 7) and Aag–/– animals (n = 18). Data are mean ± SD. (D) Pathology scores for Aag+/+ (circles) and Aag–/– (diamonds) mice. (E) Histopathology of colonic disease induced by 7 cycles of DSS. From left to right: Aag+/+ colon exhibited moderate inflammation and glandular epithelial hyperplasia; Aag+/+ colon exhibited mild dysplasia characterized by epithelial cell pleomorphism and mild branching, with hyperplasia and inflammation; Aag–/– colon exhibited moderate to severe inflammation, crypt atrophy, mucosal collapse, and segmental epithelial cell loss; Aag–/– colon exhibited a portion of an intraepithelial neoplasia with mucosal dysplasia characterized by loss of columnar orientation, elongation, branching and infolding, glandular ectasia, inflammation, and crypt abscesses. Scale bars: 100 μm.