ライフサイエンスコーパス: androgen ablation therapy

1 prostate cancer progression and relapse post androgen ablation therapy.

2 burden or preventing tumor recurrence after androgen ablation therapy.

3 rounding tumor cells, particularly following androgen ablation therapy.

4 ostate-specific antigen (PSA), and secondary androgen ablation therapy.

5 recurrent prostate tumors a few years after androgen ablation therapy.

6 ependent to androgen-independent stage after androgen ablation therapy.

7 activity, which could lead to the failure of androgen ablation therapy.

8 g a novel strategy to enhance sensitivity to androgen ablation therapy.

9 hanism that allows prostate cancer to escape androgen ablation therapy.

10 metastatic disease would require palliative androgen ablation therapy.

11 ncer cells become androgen-independent after androgen ablation therapy.

12 h still occurs in many patients treated with androgen ablation therapy.

13 ate tumors from patients receiving HF during androgen ablation therapy.

14 y and metastatic human prostate cancer after androgen ablation therapy.

15 ute to the resistance of prostate cancers to androgen ablation therapy.

16 odissected (group 2B)] who had not undergone androgen ablation therapy.

17 endent stage under the selective pressure of androgen ablation therapy.

18 tions mimicking those in patients undergoing androgen ablation therapy.

19 ncer whose disease is resistant to classical androgen ablation therapies.

20 that in CaP cells from a patient who failed androgen ablation therapy, a doubly mutated AR functione

21 cally advanced or metastatic disease undergo androgen ablation therapy and most will relapse and prog

22 Prostate cancer is initially responsive to androgen ablation therapy and progresses to androgen-unr

23 ated frequently in prostate tumors following androgen ablation therapy, and Bcl-2 overexpression may

24 gen dependent disease that can be treated by androgen ablation therapy, and clinical trials are under

25 diagnosis, to detect response subsequent to androgen ablation therapy, and to detect recurrence.

26 cer growth and progression, especially after androgen ablation therapy, are poorly understood.

27 Although the current androgen ablation therapy can repress the expression of

28 Current androgen ablation therapies for prostate cancer are init

29 be crucial for development of resistance to androgen ablation therapy for PCa.

30 ts showed no activation of MAP kinase before androgen ablation therapy; however, following androgen a

31 h factor pathways may explain the failure of androgen ablation therapies in some cases, there is litt

32 A re-elevation and hormone resistance during androgen ablation therapy in prostate cancer patients.

33 ial for monitoring the therapeutic effect of androgen ablation therapy in prostate cancer.

34 aises a concern for using HF in the complete-androgen-ablation therapy in prostate cancer treatment a

35 Androgen ablation therapy induces apoptosis only in andr

36 Androgen ablation therapy induces expression of constitu

37 ent to an androgen-independent tumor, making androgen ablation therapy ineffective.

38 with metastatic prostate cancer who undergo androgen-ablation therapy invariably relapse and develop

39 Androgen ablation therapy is effective in treating andro

40 Androgen ablation therapy is effective in treating andro

41 Although androgen ablation therapy is effective in treating prima

42 Androgen ablation therapy is eventually followed by a mo

43 Relapse of prostate cancer after androgen ablation therapy is hormone-refractory, with co

44 Progression to CRPC after androgen ablation therapy is predominantly driven by der

45 ial response of a prostate cancer patient to androgen ablation therapy is regression of the disease.

46 ients with metastatic disease who had failed androgen ablation therapy, more than 90% of the primary

47 ostate cancer initially respond favorably to androgen ablation therapy, most experience a relapse of

48 red with 3D-CRT alone or in combination with androgen ablation therapy, no severe toxicities were enc

49 n to an androgen-independent state following androgen ablation therapy, prostate cancer cells continu

50 The mechanism(s) that underlie resistance to androgen ablation therapy remain mostly unknown.

51 omponents in the initiation and evolution of androgen ablation therapy resistance in prostate cancer.

52 ound in patients whose cancer relapsed after androgen ablation therapy, supporting the idea that AR b

53 endent prostate cancer is available, whereas androgen ablation therapy, surgery, and radiation therap

54 atly increased in prostate carcinomas during androgen ablation therapy that correlates with hormone-r

55 ion analysis of human prostate cancer during androgen ablation therapy to identify genes regulated by

56 lar carcinoma (HCC) remain controversial and androgen ablation therapy to treat HCC also leads to inc

57 However, after androgen ablation therapy, tumors relapse to an androgen

58 tumor cells should prolong the usefulness of androgen ablation therapy, we determined if androgen-ind

59 Androgen ablation therapy, which may result in programme

60 pression of c-MYC (Hi-Myc mice) subjected to androgen ablation therapy with bicalutamide.

61 zed four prostate cancer patients undergoing androgen ablation therapy with flutamide and compared th