Combination of RCPNs and ADR could suppress the tumor growth more efficiently than using ADR only on mouse xenograft model bearing ADR resistant human breast cancer.
By contrast, no changes in [18F]FLT uptake were observed in mice bearing the resistant cell line H1975 or in the control group treated with the vehicle alone (Fig. 2A).
On the basis of these observations, here, we tested whether early changes of the 18F-FDG uptake in animal models bearing erlotinib-resistant NSCLC may have different imaging patterns of response to erlotinib depending on the molecular mechanism underlying resistance.
Interestingly, we found that vemurafenib treatment in mice bearing drug-resistant A375 xenografts also induced increased FDG tumor uptake, accompanied by increases in Hif-1α, Sp1 and Ksr protein levels.
Darolutamide significantly inhibited cell growth and AR transcriptional activity in enzalutamide-resistant MR49F cells in vitro, and led to decreased tumor volume and serum prostate-specific antigen levels in vivo, prolonging survival in mice bearing enzalutamide-resistant MR49F xenografts.
Nude mice bearing erlotinib-resistant H1975 and H1993 xenografts (four animals for each cell line and for each treatment) were subjected to 18F-FDG PET/CT scan before and immediately after treatment (50 mg/kg p.o. for 3 days) with erlotinib, WZ4002, crizotinib, or vehicle.
The aim of the present study was to test whether early changes of 18F-fluorodeoxyglucose (18F-FDG) uptake in animal models bearing erlotinib-resistant NSCLC may have different imaging patterns of response to erlotinib depending on the molecular mechanisms underlying resistance.
For example, the combination of vorinostat and TRAIL resulted in significant growth inhibition when compared with either treatment alone in mice bearing TRAIL-resistant tumor xenografts [ 28].
Consistent with this, we did not detect dulanermin-dependent increases in circulating cell-death markers in either mice bearing dulanermin-resistant tumourous or non-tumour-bearing mice (Supplementary Figure 1).
By 12 days following the last treatment, all mice bearing ADR-resistant tumours had died (or were terminated because of excessive tumour size), as had mice bearing ADR-sensitive tumours treated with PBS.
