ライフサイエンスコーパス: androgen-independent prostate cancer

1 lly, FGF8 expression was shown to persist in androgen independent prostate cancer.

2 ay increase BZ effectiveness in treatment of androgen-independent prostate cancer.

3 androgen receptor (AR) and the emergence of androgen-independent prostate cancer.

4 e mice bearing s.c. xenografts of PC-3 human androgen-independent prostate cancer.

5 n made in the treatment and understanding of androgen-independent prostate cancer.

6 and development of treatment for metastatic androgen-independent prostate cancer.

7 This combination is active in men with androgen-independent prostate cancer.

8 sults in the transition to a more aggressive androgen-independent prostate cancer.

9 inform novel methods to block AR function in androgen-independent prostate cancer.

10 at altered p44 expression is associated with androgen-independent prostate cancer.

11 ay be a potential target for therapy against androgen-independent prostate cancer.

12 C subfamily, is linked to the development of androgen-independent prostate cancer.

13 provide new, targeted specific therapies for androgen-independent prostate cancer.

14 ed drug development against human metastatic androgen-independent prostate cancer.

15 ults suggest a novel therapy for AR-positive androgen-independent prostate cancer.

16 ticosteroids improves survival in metastatic androgen-independent prostate cancer.

17 ndrogen receptor continues to play a role in androgen-independent prostate cancer.

18 ic pathways for the therapeutic targeting of androgen-independent prostate cancer.

19 l included a large fraction of patients with androgen-independent prostate cancer.

20 t extending survival in men with progressive androgen-independent prostate cancer.

21 losely correlated with tumor progression and androgen-independent prostate cancer.

22 mbination with radiation or chemotherapy for androgen-independent prostate cancer.

23 rt for this approach in men with metastatic, androgen-independent prostate cancer.

24 have been reported to be useful in advanced androgen-independent prostate cancer.

25 en has been implicated in the progression of androgen-independent prostate cancer.

26 well tolerated in patients with progressive androgen-independent prostate cancer.

27 ts as a survival and migratory factor(s) for androgen-independent prostate cancers.

28 eased transcriptional activation reported in androgen-independent prostate cancers.

29 A-PCa-2b human androgen-sensitive and DU-145 androgen-independent prostate cancers.

30 tivation of HER2 receptor tyrosine kinase in androgen-independent prostate cancers.

31 f phase II clinical trials for patients with androgen-independent prostate cancer (AIPC) have used PS

32 present there is no effective treatment for androgen-independent prostate cancer (AIPC).

33 nd thalidomide have demonstrated activity in androgen-independent prostate cancer (AIPC).

34 in PSA level of > or =50%) in 15% to 30% of androgen-independent prostate cancer (AiPCa) patients.

35 prostate cancer (ADPCa) and 37 patients with androgen-independent prostate cancer (AIPCa) were treate

36 Patients with progressive metastatic androgen-independent prostate cancer and adequate organ

37 e risk of skeletal complications in men with androgen-independent prostate cancer and bone metastases

38 bitors (CKIs) are associated with aggressive androgen-independent prostate cancer and contribute to u

39 TKs play an important role in the biology of androgen-independent prostate cancer and provide a ratio

40 ts demonstrate that GHRH antagonists inhibit androgen-independent prostate cancers and, after combina

41 his tumor progression, gene expression in 33 androgen-independent prostate cancer bone marrow metasta

42 ts androgen receptor-mediated cell growth in androgen-independent prostate cancer by disrupting the a

43 identify leptin as a novel growth factor in androgen-independent prostate cancer cell growth.

44 bone sialoprotein promoter activities in an androgen-independent prostate cancer cell line of LNCaP

45 We found that the androgen-independent prostate cancer cell line PC-3 unde

46 The response to cAMP is different in the androgen-independent prostate cancer cell line PC-3, whe

47 and transcript in the high Bcl-2-expressing, androgen-independent prostate cancer cell line, by all-t

48 neuroendocrine differentiation in DU145, an androgen-independent prostate cancer cell line.

49 ed at significantly higher levels in several androgen-independent prostate cancer cell lines (PC3, DU

50 itive prostate cancer LNCaP cells but not in androgen-independent prostate cancer cell lines DU145 an

51 ostate tumor tissue samples and in the human androgen-independent prostate cancer cell lines PC-3 and

52 rBbKIm may be explored for investigating the androgen-independent prostate cancer cell lines PC3 and

53 aled markedly decreased USF2 levels in three androgen-independent prostate cancer cell lines, PC-3, D

54 was elevated in the secretomes of all of the androgen-independent prostate cancer cell lines, with no

55 growth factor that stimulates the growth of androgen-independent prostate cancer cell lines.

56 cally reduces IL-6 promoter activity in both androgen-independent prostate cancer cell lines.

57 ulation of connexins was observed in several androgen-independent prostate cancer cell lines.

58 d the biological effects of Frzb/sFRP3 on an androgen-independent prostate cancer cell model.

59 rgistic effects on the leptin stimulation of androgen-independent prostate cancer cell proliferation,

60 tumor-derived AR mutant (T877A), leading to androgen-independent prostate cancer cell proliferation.

61 activation is required for leptin-mediated, androgen-independent prostate cancer cell proliferation.

62 ion of JNK blocked the leptin stimulation of androgen-independent prostate cancer cell proliferation.

63 weight homeostasis cooperate with leptin in androgen-independent prostate cancer cell proliferation:

64 fic inhibitor, ISO-1) were only effective in androgen-independent prostate cancer cells (DU-145), res

65 e, degrade, and inhibit both AR and AR-V7 in androgen-independent prostate cancer cells and highlight

66 avir, inhibited the growth of DU145 and PC-3 androgen-independent prostate cancer cells as measured b

67 BMD188 kills androgen-independent prostate cancer cells as well as pr

68 The molecular basis for androgen-independent prostate cancer cells behaving like

69 d viability of androgen-sensitive as well as androgen-independent prostate cancer cells both in vitro

70 nhibits total AR transcriptional activity in androgen-independent prostate cancer cells expressing bo

71 the GHRH antagonist, JMR-132, on PC-3 human androgen-independent prostate cancer cells in vitro and

72 in the tumors, targeted the cell surface of androgen-independent prostate cancer cells in vitro, and

73 ed the growth of both androgen-dependent and androgen-independent prostate cancer cells irrespective

74 urther investigated in vitro using the human androgen-independent prostate cancer cells PC-3 and the

75 appaB p50 and p65 and AP-1 JunD and Fra-1 in androgen-independent prostate cancer cells results in de

76 the endogenous expression status of MEK5 in androgen-independent prostate cancer cells upon recombin

77 triguingly, leptin induces JNK activation in androgen-independent prostate cancer cells, and the phar

78 androgen-dependent, as well as AR-sensitive androgen-independent prostate cancer cells, to growth in

79 cells but also acts as a tumor inhibitor for androgen-independent prostate cancer cells.

80 to identify the degraders of AR and AR-V7 in androgen-independent prostate cancer cells.

81 lly expressed on both androgen-dependent and androgen-independent prostate cancer cells.

82 ion, prostate cancer growth, and invasion in androgen-independent prostate cancer cells.

83 RGS2 as a gene specifically downregulated in androgen-independent prostate cancer cells.

84 l differences between androgen-dependent and androgen-independent prostate cancer cells.

85 oter and MEF2C transcriptional activities in androgen-independent prostate cancer cells.

86 ional level in androgen-dependent but not in androgen-independent prostate cancer cells.

87 elements involved in IL-6 gene expression in androgen-independent prostate cancer cells.

88 ole in regulating the growth and survival of androgen-independent prostate cancer cells.

89 growth arrest in both androgen-dependent and androgen-independent prostate cancer cells; however, lon

90 Androgen-independent prostate cancers, correlated with h

91 Mechanisms underlying progression to androgen-independent prostate cancer following radical a

92 nude mice bearing xenografts of DU-145 human androgen-independent prostate cancer for 8 weeks with po

93 herefore, IL-8 is a molecular determinant of androgen-independent prostate cancer growth and progress

94 Endostatin inhibits androgen-independent prostate cancer growth by suppressi

95 It is widely suspected that androgen-independent prostate cancer growth depends on a

96 been investigating the mechanisms underlying androgen-independent prostate cancer in Nkx3.1;Pten muta

97 oglobulin are highly active in osteoblastic, androgen-independent prostate cancer in vivo.

98 f PC-3 cells, which are derived from a human androgen-independent prostate cancer, into cells with a

99 fective treatment for patients with advanced androgen-independent prostate cancer is available, where

100 molecules involved in the transformation to androgen-independent prostate cancer is essential for th

101 The onset of the androgen-independent prostate cancer is often associated

102 e causal role of these downstream kinases in androgen-independent prostate cancers is unknown.

103 Androgen-independent prostate cancer leads to significan

104 consider the possibility that the growth of androgen-independent prostate cancers might be reduced b

105 In the treatment of androgen-independent prostate cancer, oral premarin has

106 tyrosine kinases as the growth mediators of androgen-independent prostate cancer; overexpression of

107 ress neutral endopeptidase (NEP), but not in androgen-independent prostate cancer (PC) cells, which l

108 es neuropeptides implicated in the growth of androgen-independent prostate cancer (PC).

109 es neuropeptides implicated in the growth of androgen-independent prostate cancer (PC).

110 esin, which are implicated in progression to androgen-independent prostate cancer (PC).

111 blocking its metabolism inhibits invasion of androgen-independent prostate cancer (PC-3 and DU-145) c

112 BZ unexpectedly increases IL-8 expression in androgen-independent prostate cancer PC3 and DU145 cells

113 y chain (MRC) in BMD188-induced apoptosis in androgen-independent prostate cancer PC3 cells and compa

114 ulated gene expression during progression of androgen-independent prostate cancer (PCa) and metastati

115 is expressed in both androgen-dependent and androgen-independent prostate cancer (PCa) cells, wherea

116 role of androgen receptor (AR) mutations in androgen-independent prostate cancer (PCa) was determine

117 oxia-reoxygenation may select for aggressive androgen-independent prostate cancer phenotype.

118 LEF1 is highly expressed in androgen-independent prostate cancer, potentially servin

119 not LH, may directly stimulate the growth of androgen-independent prostate cancer, suggesting that pe

120 ughout the course of prostate cancer and, in androgen-independent prostate cancer, takes on the role

121 prostate cancer, but eventually progressing androgen-independent prostate cancer threatens the lives

122 5-156 may inhibit the growth of DU-145 human androgen-independent prostate cancers through a reductio

123 ion of bone pain can be achieved in men with androgen-independent prostate cancer treated with doceta

124 uman cell lines encompassing the spectrum of androgen-independent prostate cancers was compared with

125 Patients with progressive, androgen-independent prostate cancer were randomly assig

126 2 was examined in a human xenograft model of androgen-independent prostate cancer where BBL22 signifi

127 shown promising efficacy in the treatment of androgen-independent prostate cancer, with significantly

128 TMPRSS2 as a gene that is down-regulated in androgen-independent prostate cancer xenograft tissue de

129 ficantly suppressed the growth of PC-3 human androgen-independent prostate cancers xenografted into n

130 We also demonstrate that androgen-independent prostate cancer xenografts have hig