Extended Data Fig. 9: NK cells suppress gastric cancer metastasis to the liver.

(a) Primary tumor weights of a random subset of mice from Fig. 6d (IgG n = 4 mice; α-NK1.1 n = 6 mice). (b, c) Hematoxylin and eosin (H&E) staining of liver metastases of C57BL/6 MYC-Apc^−/− EPO-GEMMs treated with an NK1.1-targeting antibody or the respective IgG control directly before tumor initiation (B) (representative image of n = 7 mice) or after palpable tumor formation (C) (representative image of n = 8 mice). (d) H&E staining of livers of C57BL/6 mice after tail vein injection of MYC-Apc^−/− gastric cancer cells and treatment with either an antibody targeting NK1.1 (right) or IgG control (left) (representative images of n = 8–9 mice per group). (e) Quantification of the number of liver metastases (left) and the percentage area of total liver occupied by the metastasis (right) from mice in (D) (n = 8 independent mice). (f) H&E staining of livers of C57BL/6 mice after splenic injection of MYC-Apc^−/− gastric cancer cells and treatment with either an antibody targeting NK1.1 (right) or IgG control (left). Representative images of n = 12–14 mice per group. (g) Quantification of the number of liver metastases (left) and the percentage area of total liver occupied by the metastases (right) from mice in (F) (n = 12 independent mice). (h) Quantification of the percentage area of total lung occupied by metastases in a randomly chosen subset of R2G2 mice from Fig. 7b (MSS n = 7 mice; MSI n = 6 mice). Statistical analysis: (A), (E), (G), (H) two-tailed Mann–Whitney U-test. Data are presented as mean values +/− s.e.m.

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