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. 2021 Dec 20;126(6):927–936. doi: 10.1038/s41416-021-01652-y

Fig. 4. Use of the CSF-1R active inhibitor GW2580 prevents differentiation of HSPCs into M2 macrophages after RT reducing tumour regrowth.

Fig. 4

a The effects of treating tumour bearing mice with SRT and GW2580 show that each treatment alone or in combination resulted in smaller tumour volumes in comparison to non-treated controls. *p < 0.05 in comparison to NRT-treated tumours; #p < 0.05 in comparison to GW2580 and SRT alone (n = 7). b Western blot analysis demonstrates both the ability of GW2580 to inhibit CSF-1R phosphorylation during dose delivery and the loss of inhibition after dose withdrawal. The fold changes for the densitometry measurements, normalised to β-actin and then compared to NRT controls, are indicated below the corresponding lane. Numbers without brackets compare day 6 changes (n = 3); numbers with brackets compare day 12 changes (n = 6); ND denotes “not detected”. c–e RT-PCR analysis shows that use of GW2580 has no effect on CSF-1 production (c), results in tumour maintenance of CD133+ HSPCs (d), and decreased levels of M2 macrophages (e) (day 6 n = 3, day 12 n = 6). f Tumours significantly regrow after withdrawal of GW2580 from tumour bearing mice (n = 4). *p < 0.05 for indicated comparisons, no animals were excluded from analysis, relative gene expression values were normalised to both TBP (housekeeping gene) and NRT day 6 values.