Figure 5.
Figure 5. In vivo molecular profiling of hsp90 inhibition. MM-1S-GFP+/Luc+ cells injected intravenously in SCID/NOD mice led to development of diffuse bone lesions. Mice were randomly assigned to receive either a single dose of 17-AAG (50 mg/kg intraperitoneally) or vehicle; 24 hours after drug administration, all mice were humanely were killed and GFP+ MM bone lesions were visualized during necropsy by whole-body fluorescence imaging and harvested for further molecular analyses. (A) Flow cytometric analysis documents significant suppression of IGF-1R cell surface expression in MM tumor cells from 17-AAG-treated mice, compared to control mice. Filled curves correspond to staining with anti-IGF-1R antibody; open curves, staining with isotype control. (B) Hierarchical clustering analysis of in vivo gene expression profiles of MM-1S cells in 17-AAG-treated versus control mice.

In vivo molecular profiling of hsp90 inhibition. MM-1S-GFP+/Luc+ cells injected intravenously in SCID/NOD mice led to development of diffuse bone lesions. Mice were randomly assigned to receive either a single dose of 17-AAG (50 mg/kg intraperitoneally) or vehicle; 24 hours after drug administration, all mice were humanely were killed and GFP+ MM bone lesions were visualized during necropsy by whole-body fluorescence imaging and harvested for further molecular analyses. (A) Flow cytometric analysis documents significant suppression of IGF-1R cell surface expression in MM tumor cells from 17-AAG-treated mice, compared to control mice. Filled curves correspond to staining with anti-IGF-1R antibody; open curves, staining with isotype control. (B) Hierarchical clustering analysis of in vivo gene expression profiles of MM-1S cells in 17-AAG-treated versus control mice.

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