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. 2017 Apr 7;8:14922. doi: 10.1038/ncomms14922

Figure 2. Lkb1 deletion after transplant of KRAS adenocarcinoma cells drives SCC transition.

Figure 2

(a) Schematic of adenocarcinoma induction, transplantation and deletion of Lkb1 in recipient mice. (b) Haematoxylin and eosin staining of transplanted KRAS tumours show only adenocarcinoma histology, while ADSCC and SCC were visible in tamoxifen-treated mice, scale bar, 50 μm. (c) Percentage of mice with at least one purely squamous lesion as determined by histology at end point in the four cohorts, n and P values indicated in the figure, P values represent χ2-test. (d) Representative flow cytometric plot of dissociated tumours from untreated (no tamoxifen) transplanted KRAS tumours (top) and tamoxifen-treated mice (bottom) gated on DAPI/CD31/CD45/EpCAM+ cells and showing NGFR and Sca1 staining. (e) Haematoxylin and eosin staining tumours derived from transplanted Sca1HighNGFRHigh or Sca1HighNGFRLow cells from an SCC KRAS/Lkb1 lesion demonstrates that the switch to the squamous phenotype is stable, scale bar, 50 μm. See also Supplementary Fig. 2a–c.