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1 ic siRNA or androgen inhibitor bicalutamide (Casodex).
2 ot in LNCaP-cdxR cells (GI(50)=24+/-5 microM Casodex).
3 ium and in the presence of the AR-antagonist Casodex.
4 These effects can be reversed by casodex.
5 sed both by androgens and by the antagonist, Casodex.
6 ctivated by agonist, was obliterated only by Casodex.
8 the observation that W-7 was as effective as Casodex, an antiandrogen, in blocking AR-regulated expre
9 e treatment of synchronized LNCaP cells with Casodex, an AR-antagonist, for 4 hours in mid-G(1) phase
10 ase in the survival of cells co-treated with Casodex and ATM inhibitor as compared with those treated
11 ication 3-fold, whereas androgen inhibitors (casodex and flutamide) suppressed viral growth up to 3-f
13 d AR was required because the AR antagonists casodex and hydroxyflutamide failed to translocate beta-
14 like the clinically important antiandrogens, casodex and hydroxyflutamide, both D36 and D80 block and
15 growth-inhibitory action of the antiandrogen Casodex and inhibits anchorage-independent cell growth.
18 nt study, we observed that the AR antagonist Casodex (bicalutamide) disrupted telomeric complexes in
19 ffects of the currently used anti-androgens, Casodex/bicalutamide and MDV3100/enzalutamide, and the n
21 ibitory potencies were comparable to that of casodex but remarkably superior to that of flutamide.
22 rvations in LNCaP cells (GI(50)=6+/-3 microM Casodex) but not in LNCaP-cdxR cells (GI(50)=24+/-5 micr
23 tiandrogens, hydroxyflutamide, bicalutamide (casodex), cyproterone acetate, and RU58841, and other co
24 of cells from G(1) to S phase, the effect of Casodex during mid-G(1) suggested that the role of AR in
25 hydroxyflutamide (Eulexin) and bicalutamide (Casodex), fail to block completely the Adiol-induced and
26 ivity under these conditions; treatment with Casodex has the potential to counteract this induction.
27 ocked by an anti-androgen drug bicalutamide (Casodex), implicating the involvement of androgen recept
31 l of AIPC cells was found to be resistant to Casodex-induced growth inhibition, but with the exceptio
32 th untreated controls, and the antiandrogen, casodex, inhibited the mibolerone-stimulated increase in
34 cancer cells and suggest that AR-antagonist Casodex-mediated cell death may be due to telomere compl
36 ptor (AR) in these cells by the antiandrogen casodex or by the anti-AR small interfering RNA inhibite
38 nction in cells treated with AR-antagonists (Casodex or MDV3100) or AR-siRNA was associated with a dr
39 MAPK) kinase (MEK); or (c) the antiandrogen, Casodex; or when the cells were cultured under androgen-
41 hesized compounds, (R)-16m, when compared to casodex, (R)-bicalutamide, and enzalutamide, displayed v
42 The use of the antiandrogen bicalutamide (Casodex) rescued LNCaP cells from 5-alpha-dihydrotestost
44 ivation of Akt indicating that FlnA restored Casodex sensitivity in C4-2 cells by decreasing Akt phos
46 ydroxyflutamide (Eulexin), and bicalutamide (casodex), that are widely used for the treatment of pros
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