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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.
7          This androgen effect was blocked by Casodex, an androgen receptor blocker.
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
12                   Two potent anti-androgens, casodex and flutamide, can significantly reduce this act
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.
16 is action was inhibited by the AR antagonist Casodex and MEK-1 inhibitor PD98059.
17  by the synthetic antiandrogen bicalutamide (Casodex) at the same concentration.
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
20                             The antiandrogen Casodex blocked the effect of androgen, implicating the
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
28                 Fisetin also synergized with Casodex in inducing apoptosis in LNCaP cells.
29 but not control siRNA, induced resistance to Casodex in LNCaP cells.
30 mparison with the antiandrogen bicalutamide (Casodex) in AIPC cells.
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
33         Mechanism dissection indicated these Casodex/MDV3100 treatments enhanced the TGF-beta1/Smad3/
34  cancer cells and suggest that AR-antagonist Casodex-mediated cell death may be due to telomere compl
35 r as compared with those treated with either Casodex or ATM inhibitor alone.
36 ptor (AR) in these cells by the antiandrogen casodex or by the anti-AR small interfering RNA inhibite
37          In vitro results showed that 10 mum Casodex or MDV3100 treatments suppressed PCa cell growth
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-
40         Using the antiandrogen Bicalutamide (Casodex((R))), which slows down AR activation and nuclea
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
43                     In LNCaP cells and their Casodex-resistant derivative, LNCaP-cdxR, growth inhibit
44 ivation of Akt indicating that FlnA restored Casodex sensitivity in C4-2 cells by decreasing Akt phos
45 tion in androgen-reduced medium and restored Casodex sensitivity.
46 ydroxyflutamide (Eulexin), and bicalutamide (casodex), that are widely used for the treatment of pros
47                               In response to Casodex, there were similar observations in LNCaP cells
48 zed and co-immunoprecipitated with Cdc6, and Casodex treatment disrupted this interaction.
49 itulated the action of hormone; accordingly, Casodex was a poor antagonist of the synergy.
50                                    Moreover, Casodex washout led to the reversal of telomere dysfunct

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