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. Author manuscript; available in PMC: 2019 Aug 27.
Published in final edited form as: Science. 2018 Dec 21;362(6421):1416–1422. doi: 10.1126/science.aas9090

Fig. 4. Combination trametinib and palbociclib treatment drives NK cell–mediated lung tumor regressions in genetically engineered mice.

Fig. 4.

(A) Immunohistochemical staining of KP GEMM tumors treated with vehicle or combined trametinib (1 mg/kg body weight) and palbociclib (100 mg/kg body weight) for 2 weeks (scale bar, 50 μm). CC3, cleaved caspase-3; pERK, phosphorylated extracellular signal–regulated kinase. (B) Representative μCT images of KP GEMM lung tumors prior to treatment and after 2 weeks of treatment with vehicle or combined trametinib (1 mg/kg body weight) and palbociclib (100 mg/kg body weight) and either an isotype control antibody (C1.18.4) or NK1.1 depleting antibody (PK136). Yellow boxes indicate lung tumors. (C) A waterfall representation of the response of each tumor after 2 weeks of treatment with vehicle, trametinib (1 mg/kg body weight), palbociclib (100 mg/kg body weight), or both, and either an isotype control (C1.18.4), NK1.1 (PK136), TNF-α (XT3.11), or ICAM-1 (YN1/1.7.4) blocking antibody (n ≥ 6 per group). (D) Kaplan-Meier survival curve of KP GEMM mice treated as in (C) (n ≥ 6 per group) (log-rank test). (C) One-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.