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1 approach for extending clinical responses to antiandrogen therapy.
2 ve an inferior response to second-generation antiandrogen therapy.
3 Survivin via AKT could mediate resistance to antiandrogen therapy.
4 upporting a novel mechanism of resistance to antiandrogen therapy.
5 ciated with the development of resistance to antiandrogen therapy.
6  cells resistant to androgen ablation and/or antiandrogen therapy.
7 tients treated with androgen ablation and/or antiandrogen therapy.
8 om a patient with disease progression during antiandrogen therapy.
9 eficiency was apparent in patients receiving antiandrogen therapy.
10         BAT can sensitize CRPC to subsequent antiandrogen therapy.
11 gy to enhance prostate cancer sensitivity to antiandrogen therapy.
12 therapy-resistant PCa compared with standard antiandrogen therapy.
13 rogen receptor expression and sensitivity to antiandrogen therapy.
14 dditional loss of Trp53 causes resistance to antiandrogen therapy.
15 pment of resistance to androgen ablation and antiandrogen therapies.
16 g those resistant to androgen deprivation or antiandrogen therapies.
17 many skin conditions clinically improve with antiandrogen therapies.
18 d AR protein levels, fostering resistance to antiandrogen therapies.
19  and potentially extend clinical response to antiandrogen therapies.
20 undergo radiation therapy and receive either antiandrogen therapy (24 months of bicalutamide at a dos
21                                    Immediate antiandrogen therapy after radical prostatectomy and pel
22 mly assigned patients who had never received antiandrogen therapy and who had distant metastases from
23 de treatment is poorly responsive to further antiandrogen therapy, and paradoxically, rapid cycling b
24        Strategies to enhance the efficacy of antiandrogen therapy are needed.
25  or protein restriction, in combination with antiandrogen therapy as a treatment for prostate cancer.
26 that Survivin can mediate resistance to such antiandrogen therapies based on our assays.
27               Prostate cancer relapsing from antiandrogen therapies can exhibit variant histology wit
28               Although initially successful, antiandrogen therapy eventually fails and androgen deple
29 use the optimal timing of the institution of antiandrogen therapy for prostate cancer is controversia
30 mechanism of resistance to second-generation antiandrogen therapy, highlighting the therapeutic poten
31 strategy for sequencing between androgen and antiandrogen therapies in metastatic castration-resistan
32    It is hypothesized that administration of antiandrogen therapy in an intermittent, as opposed to c
33                                Resistance to antiandrogen therapy in patients with metastatic prostat
34 eting of Survivin may enhance sensitivity to antiandrogen therapy in prostate cancer.
35 aling and will respond to potent second-line antiandrogen therapies, including bicalutamide (CASODEX(
36 -free survival rate for the CRPC patients on antiandrogen therapies is only 8-19 months.
37                                              Antiandrogen therapy is only palliative, and chemotherap
38 on therapy, brachytherapy, and cryosurgery), antiandrogen therapy management of erectile dysfunction,
39                                 Nonsteroidal antiandrogen therapy may be discussed as an alternative,
40 , for condition two, the treatment effect of antiandrogen therapy on MFS and OS were correlated (R(2)
41  in detection efficacy was present regarding antiandrogen therapy (P = 0.0783).
42 llular plasticity that, when challenged with antiandrogen therapy, promotes resistance through lineag
43  growth and survival and that treatment with antiandrogen therapy provides selective pressure and alt
44                                              Antiandrogen therapies reduce expression of TMPRSS2.
45 gh there has been substantial advancement in antiandrogen therapies, resistance to these treatments r
46  received chemotherapy and second-generation antiandrogen therapy, respectively.
47 either enzalutamide or standard nonsteroidal antiandrogen therapy showed an early overall survival be
48 abel enzalutamide or a standard nonsteroidal antiandrogen therapy (standard-care group).
49 rostate cancer has been transformed by novel antiandrogen therapies such as enzalutamide.
50 et for developing therapeutic agents for the antiandrogen therapy that almost always fails in the tre
51 iochemically motivated mathematical model of antiandrogen therapy that can be tested prospectively as
52            Resistance invariably develops to antiandrogen therapies used to treat newly diagnosed pro
53 which tends to be accelerated by the current antiandrogen therapy, we identify Peruvoside, a cardiac
54  and oral minoxidil, sometimes combined with antiandrogen therapy, were associated with an improvemen
55                 The addition of 24 months of antiandrogen therapy with daily bicalutamide to salvage
56                                      Whether antiandrogen therapy with radiation therapy will further
57  were randomly assigned to receive immediate antiandrogen therapy, with either goserelin, a synthetic