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1 istant disease (CRPC) when treated with anti-androgen therapy.
2 Thirty-three patients had also received androgen therapy.
3 tations in telomerase genes can improve with androgen therapy.
4 ive androgen receptor modulators (SARMs) for androgen therapy.
5 ese androgen-independent tumors despite anti-androgen therapy.
6 ncer resistance to hormone-ablative and anti-androgen therapy.
7 ese mutations may be the best candidates for androgen therapy.
8 was highest among those receiving exogenous androgen therapy.
9 ontribute to responses to supraphysiological androgen therapy.
10 direct role in preventing resistance to anti-androgen therapy.
11 and restores responsiveness of CRPC to anti-androgen therapy.
12 s, associated genetic factors, or history of androgen therapy.
13 tizing prostate cancer cells to current anti-androgen therapies.
14 apies, ERG promotes sensitivity to high-dose androgen therapy and pharmacological inhibition of wild
19 ivity, which is the basis for use of Bipolar Androgen Therapy (BAT) for patients with this disease.
21 physiological androgen (SPA), termed bipolar androgen therapy (BAT), can result in tumor regression a
23 estosterone administration, known as bipolar androgen therapy (BAT), is a treatment strategy for pati
25 w serum testosterone concentrations (bipolar androgen therapy [BAT]) in this setting might induce tum
27 blockade for prostate cancer prevention and androgen therapy for andropause treatment in elderly men
28 roendocrine (NE) cells to escape potent anti-androgen therapies however, the exact molecular events a
31 findings support the clinical evaluation of androgen therapy in the prevention and perhaps treatment
32 red physical changes from oestrogen and anti-androgen therapy include decreased body and facial hair,
33 drogens led to the development of novel anti-androgen therapies including abiraterone acetate and enz
34 ive activation that is not inhibited by anti-androgen therapies, including abiraterone or enzalutamid
37 cancers (PCs), initially responsive to anti-androgen therapies, often advance to a hormone-refractor
38 t the majority of patients treated with anti-androgen therapy progress to androgen-independence chara
39 through the transient generation of an anti-androgen therapy-resistant cell population, suggesting t
40 s, such as microRNA and prostate cancer anti-androgen therapy-resistant marker ARV7 splicing variant