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. Author manuscript; available in PMC: 2021 Dec 9.
Published in final edited form as: Cell Rep. 2021 Nov 9;37(6):109974. doi: 10.1016/j.celrep.2021.109974

Figure 1. Myc alone robustly drives tumorigenesis in Shp2-deficient liver.

Figure 1.

(A) Experimental scheme.

(B) Representative liver images and H&E staining of liver sections 4 weeks after Myc transfection with SB-11 transposase via HTVi. Liver scale bars, 0.5 cm. Staining scale bars, 500 μm.

(C–G) Quantified tumor incidences (C), liver-to-body weight ratios (LW/BW) (D), maximal tumor diameters (E), visible tumor nodule numbers (F), and spleen-to-body weight ratios (SW/BW) (G). n = 22. Values are presented as means ± SD. Statistical significance was calculated using Students’ t test (**p < 0.01, ***p < 0.001).

(H and I) Representative immunostaining of liver sections for Myc and Ki67 (H) and HNF4α and CK19 (I) 4 weeks after Myc transfection. Scale bars, 250 μm (H) and 50 μm (I).

(J) Immunoblotting of liver lysates at 0 days (0D) and 4 weeks after HTVi of Myc, using antibodies as indicated. T, tumor tissue; N, non-tumor liver tissue.

(K) Representative H&E staining of SKO liver 4 weeks post-Myc injection. For trabecular HCC with features detailed in histopathological report, see Table S1. Scale bars, 2.5 mm (top) and 100 μm (bottom 1–4). Upper box, ×4.

(L) Immunostaining of Myc, F4/80 and DAPI in WT versus SKO (tumor) 4 weeks after HTVi of Myc. Scale bars, 100 μm.