STAT3 and STAT1 mediate IL-11–dependent and inflammation-associated gastric tumorigenesis in gp130 receptor mutant mice
J. Clin. Invest. Matthias Ernst, et al. 118:1727 doi:10.1172/JCI34944 [Go to this article.]

Figure 2
Complete abrogation of gastric tumor formation in gp130^Y757F/Y757F mice lacking the IL-11Rα1 subunit. (A) Representative appearance of stomachs from 14-week-old mice. Stomachs were opened along the outer curvature and pinned out with the lumen facing the viewer. Arrows indicate macroscopically visible lesions. Fundic (f) and antral (a) stomach regions are labeled. (B) Scatter plots depicting the total mass (g) of gastric tumors for individual mice either younger or older than 14 weeks of age and belonging to the indicated genotypes. Representative H&E- (C) and proliferating cell nuclear antigen–stained (D) cross-sections through the antral region of stomachs from mice of the indicated genotypes; arrows indicate patches of inflammatory cell accumulates (C) and the defined zone of proliferating mucous neck cells of the gastric epithelium (D). Scale bars: 100 μm. F/F: 11R^–/– indicates gp130^Y757F/Y757FIl11ra1^–/– mice; F/F: 6^–/– indicates gp130^Y757F/Y757FIl6^–/– mice.