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. 2016 Feb 29;5(6):1214–1227. doi: 10.1002/cam4.670

Figure 3.

Figure 3

Host EphA4 deficiency reduced splenomegaly. (A) spleen weight was adjusted in relative to body weight of six paired tumor‐free EphA4‐KO and ‐WT mice (the same age as that of tumor‐bearing mice) and showed no significant difference after the adjustment between the two genotypes. (B,C) in the absence of IGF1 treatment, reduced splenic enlargement was found in EphA4‐KO tumor‐bearing mice compared with control ‐WT tumor‐bearing littermate mice (*P < 0.05; **P < 0.001). (B) upper lane showed dissected spleens from 5–7 week tumor‐bearing ‐WT mice; lower lane showed the spleens from 5–7 week tumor‐bearing littermate ‐KO mice without IGF1 treatment. (C) statistical analysis of B (*P < 0.05; **P < 0.001). (D) IGF1 treatment increased the spleen enlargement of EphA4‐KO tumor‐bearing mice (upper lane: from WT tumor‐bearing mice; lower lane: from littermate ‐KO tumor‐bearing mice with IGF1 treatment). (E) statistical analysis of D (*P < 0.05; **P < 0.001). (F) statistical analysis showed in the absence of IGF1 treatment, EphA4‐deleted tumor‐bearing hosts significantly reduced the splenomegaly (*P < 0.05; **P < 0.001), which was markedly enhanced by IGF1 treatment in EphA4‐KO tumor‐bearing mice; however, it could not reach the level of WT (n = 12 of ‐WT tumor‐bearing mice and n = 6 of ‐KO tumor‐bearing mice each treatment). (G) showed the comparison of spleens between tumor‐bearing and tumor‐free mice of paired EphA4‐KO and ‐WT genotype. (H) statistical analysis showed the degree of increase in spleen weight between tumor‐bearing and tumor‐free mice of paired EphA4‐KO and ‐WT genotype. The EphA4‐WT of tumor‐bearing mice showed increased splenic enlargement close to sevenfold while the ‐KO less than twofold, and IGF1 treatment enhanced multiple times.