1
Treatment of both sensitive and resistant cells with 6TG induced growth arrest.
2
Treating the resistant cells with a MEK inhibitor sensitized them to glucocorticoids.
3
Importantly, givinostat killed ruxolitinib- resistant cells and potentiated the effect of current chemotherapy.
4
Nevertheless, such treatment may lead to the selection of resistant cells.
5
In addition, increased levels of lung resistance protein were detected in imexon- resistant cells.
6
Equally obviously, those resistant cells would seem to produce an antitoxin.
7
The absence of FAK degradation may contribute to cell survival in taxane- resistant cells.
8
Accordingly, resistant cells exhibit increased exogenous FA uptake and metabolic plasticity.
9
In contrast, resistant cells show no significant changes in cell stiffness upon cisplatin treatment.
10
However, the selection of resistant cells leads to treatment failure.
11
Moreover, responses of p53 to stimulation in the TRAIL- resistant cells appeared to be impaired.
12
ICI 164384 reduced the efflux of daunomycin from resistant cells more effectively than tamoxifen.
13
These resistant cells may be effectively targeted by oHSV therapy.
14
Transfection of Apaf-1 conferred sensitivity to apoptosis in resistant cells.
15
Spared by chemotherapy, the drug- resistant cells outgrow other cancer cells.
16
Fetal liver transfer experiments suggested that TRAF6 in radiation- resistant cells is responsible for follicle formation.
