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Fig. 4 | BMC Cancer

Fig. 4

From: Upregulation of FOXM1 leads to diminished drug sensitivity in myeloma

Fig. 4

Upregulation of FOXM1 reduces susceptibility of myeloma xenografts to bortezomib in vivo. a Scheme of study design. FOXM1Hi and FOXM1N myeloma cells were generated using lentiviral gene transduction as previously described [12]. Cells were subcutaneously (s.c.) xenografted (Tx) into the right and left flank of NSG mice, respectively. Beginning on day 7 following cell transfer, 5 mice were treated with daily administrations of the proteasome inhibitor, bortezomib (Bz, 1 μg per gram body weight IV), until study termination on day 30. Five mice were left untreated. In all cases, tumor diameters were measured in 4-day intervals using a caliper, starting on day 10 after xenografting. Xenografts were harvested and weighed on a fine balance at study end. b Time course of tumor growth in host mice. Mean tumor diameters (squares) and standard deviations of the mean (short vertical lines with error bars) are plotted. In Bz-treated mice, the area under the curve (AUC) of FOXM1N tumors (148) was 13% smaller than that of FOXM1Hi (171) tumors. In untreated mice, the AUC of FOXM1N tumors (189) was 14% smaller than that of the FOXM1N (221) tumors. c Mean tumor weight at end of study. FOXM1Hi xenografts treated with Bz (1.32 ± 0.434 g) were significantly smaller than their untreated counterparts (2.40 ± 0.647 g) using Mann-Whitney’s t test (p = 0.031). FOXM1N xenografts showed the same trend (1.54 ± 0.543 g vs. 0.692 ± 0.217 g) but missed the 5% threshold of statistical significance (p = 0.056). Median tumor weights in all 4 groups were significantly different by Kruskall-Wallis analysis (p = 0.006)

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