Figure 3.
Progression of myeloma xenografts is faster in a mouse model of type 2 diabetes than without diabetes. (A) Representative MM1.S tumor xenograft growth trajectories from Rag1−/−(Rag wild-type [WT]), and Rag1−/−/MKR (Rag MKR) male mice; n = 3 to 5 per group. (B) Plasma insulin concentrations in Rag1−/− and Rag1−/−/MKR male mice; n = 3 to 5 per group. (C) Representative western blot analysis of MM1.S tumor xenograft protein lysates from Rag1−/− and Rag1−/−/MKR mice, as indicated. (D-E) Quantification of total insulin receptor expression corrected for β actin, and S6rp phosphorylation, relative to total S6rp protein levels. Results are expressed as relative difference to that of Rag1−/− mice. (F) Representative western blot analysis of MM1.S tumor cell protein lysates from with and without insulin stimulation, as indicated. (G-I) Quantification of pIR/IGF-1R, pAkt, and pS6rp relative to total protein levels; n = 3 per group. ∗P < .05 between groups; ∗∗∗P < .001, as indicated.

Progression of myeloma xenografts is faster in a mouse model of type 2 diabetes than without diabetes. (A) Representative MM1.S tumor xenograft growth trajectories from Rag1−/−(Rag wild-type [WT]), and Rag1−/−/MKR (Rag MKR) male mice; n = 3 to 5 per group. (B) Plasma insulin concentrations in Rag1−/− and Rag1−/−/MKR male mice; n = 3 to 5 per group. (C) Representative western blot analysis of MM1.S tumor xenograft protein lysates from Rag1−/− and Rag1−/−/MKR mice, as indicated. (D-E) Quantification of total insulin receptor expression corrected for β actin, and S6rp phosphorylation, relative to total S6rp protein levels. Results are expressed as relative difference to that of Rag1−/− mice. (F) Representative western blot analysis of MM1.S tumor cell protein lysates from with and without insulin stimulation, as indicated. (G-I) Quantification of pIR/IGF-1R, pAkt, and pS6rp relative to total protein levels; n = 3 per group. ∗P < .05 between groups; ∗∗∗P < .001, as indicated.

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