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. 2016 Sep 9;18(8):512–523. doi: 10.1016/j.neo.2016.07.003

Figure 3.

Figure 3

Decreased survival and increased intestinal tumor burden in ApcMin/+NHERF1−/− double-mutant mice. (A) The diagram shows the cross between NHERF1 and APC mutant mice and selection of ApcMin/+ mouse cohorts (filled circles of both male and female mice) for survival and tumor burden analysis (boxed). Kaplan-Meier survival analysis shows significantly shorter survival for ApcMin/+NHERF1−/− mice than for control ApcMin/+NHERF1+/+ mice. (B) Demographics and tumor statistical analysis in 16-week-old double-mutant and control mice shows significantly higher tumor density for ApcMin/+NHERF1−/− mice in the small intestine (SI) for both males (M) and females (F), and in the colon for females. Data are means ± SEM. *P < .05; **P < .01; ***P < .005. (C) Swiss-roll H&E histology of distal SI and colon from two females in (B). Arrows indicate some of the polyps. Note higher tumor density and larger adenomas in ApcMin/+NHERF1−/− intestine compared to control. (D–F) Tumor-count statistics performed as in (B) to demonstrate tumor regional distribution in the SI per genotype (D), adenoma numbers in the whole intestine in all mice and per gender (E), and adenoma distribution of sizes in the whole intestine (F). Adenomas were defined as tumors with diameter larger than 1 mm. The regional distribution of very large adenomas (>2.5 mm) is also shown in (F).