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. Author manuscript; available in PMC: 2017 Apr 1.
Published in final edited form as: Gastroenterology. 2015 Dec 8;150(4):918–930.e13. doi: 10.1053/j.gastro.2015.11.049

Figure 5. Regression of Kras-induced metaplasia by MEK inhibition.

Figure 5

A) Selumetinib treatment schematic. At 3 months post tamoxifen treatment, Mist1-Kras-mTmG mice were treated with either DMSO (n=5) or 2 mg/kg Selumetinib (n=4) once daily for 2 weeks. B) Top row: H&E stained stomachs from mice treated with DMSO or with Selumetinib. DMSO treated mice showed severe metaplasia (arrow), but normal mucosal cells were observed in glands of Selumetinib-treated mice (arrows). Sections of the corpus from DMSO or Selumetinib treated mouse stomachs were immunostained with antibodies against GFP (green) and H/K-ATPase (red) (middle row) or with antibodies against CD44v (green), Ki67 (red) and intrinsic factor (blue), and GSII-lectin (white) (bottom row). DAPI was used for nuclear staining. Mucous neck cells (GSII+/CD44v−, white arrow) and chief cells (IF+/CD44v−, yellow arrow) were also observed in the Selumetinib-treated mice. Yellow dotted lines indicate the junction of zones between proliferating metaplastic cells and normal progenitor cells. Boxes indicate regions enlarged. Scale bars = 100 μm.