ライフサイエンスコーパス: anti-estrogen

1 eceptor-alpha (ERalpha) and are treated with anti-estrogens.

2 ing sensitivity to the inhibitory effects of anti-estrogens.

3 The anti-estrogen 4-hydroxytamoxifen blocks Rsk2-mediated ac

4 , ER(+) cells also acquire resistance to the anti-estrogen 4-hydroxytamoxifen due to the rise of cycl

5 al estrogen receptors, as it is abrogated by anti-estrogen administration.

6 ffects of estrogen agonists and antagonists (anti-estrogens [AE]) on growth of MM cell lines and MM p

7 Endoxifen is known to be a potent anti-estrogen and its mechanisms of action are still bei

8 g domain is required for repression, because anti-estrogens and AF-2 mutations impair repression.

9 ain (LBD), all of whom had been treated with anti-estrogens and estrogen deprivation therapies.

10 predictive of the clinical effectiveness of anti-estrogens and, as a result, downstream metabolic re

11 The effects of the anti-estrogen, anion channel blocker, tamoxifen on amino

12 ailable on biphosphonates, ovarian ablation, anti-estrogens, anti-HER-2 (human epidermal growth facto

13 Anti-estrogens are a prime example of a targeted therapy

14 While anti-estrogens/aromatase inhibitors are initially effect

15 ive cell line as treatment of the cells with anti-estrogen-blocked cell death.

16 prostate-specific antigen was not blocked by anti-estrogens, but was blocked both by anti-androgens a

17 alpha, which in turn increases TAM-dependent anti-estrogen chemosensitivity in vitro and in vivo.

18 ls expressed estrogen receptors and the pure anti-estrogen compound, ICI 182780, did not induce apopt

19 ing resulted in decreased sensitivity to the anti-estrogen drug Tamoxifen but increased expression of

20 poptosis in response to staurosporine or the anti-estrogen drug tamoxifen.

21 Based on our recent finding of anti-estrogen/ER-beta-mediated growth inhibition of pros

22 Moreover, anti-estrogens frequently activate several signaling cas

23 for MED1 in mediating resistance to the pure anti-estrogen fulvestrant both in vitro and in vivo.

24 Pure anti-estrogen fulvestrant has been shown to be a promisi

25 uppression of migration was inhibited by the anti-estrogen ICI 164,384 and the gene transcription inh

26 eptor antagonist 4-Hydroxy-Tamoxifen and the anti-estrogen ICI 164383.

27 receptor alpha (ERalpha) and reversed by the anti-estrogen ICI 182, 780, and this response was not af

28 the inhibitory effects of treatment with the anti-estrogen ICI 182,780 on CXCR4-mediated tumor growth

29 CF-7 cells with the PFKFB3 inhibitor and the anti-estrogen ICI 182,780 synergistically induces apopto

30 kinase and MAPK activity, are blocked by the anti-estrogen ICI 182,780.

31 nists, estrogen, diethylstilbestrol, and the anti-estrogen ICI 182780 on cellular degradation of 3H-l

32 llowing ovariectomy or following exposure to anti-estrogen implanted directly into the gland.

33 tein expression is inducible by estrogen and anti-estrogens in ER-positive breast cancer cells.

34 gen treatment and plays an important role in anti-estrogen induced apoptosis of breast cancer cells.

35 Anti-pan-TGF-beta antibodies did not block anti-estrogen-induced recruitment in G1 and inhibition o

36 the deregulation of FOXM1 may contribute to anti-estrogen insensitivity.

37 ogated the cell cycle arrest mediated by the anti-estrogen OHT.

38 her, effects of estrogens or highly specific anti-estrogens on bone turnover do not support the hypot

39 shown that estrogen inhibits Notch, whereas anti-estrogens or estrogen withdrawal activate Notch sig

40 ogens on early mesenchymal cell progenitors, anti-estrogen receptor-alpha (anti-ER alpha) Ab's stain

41 Because anti-estrogens reduced PTTG expression in human pituitar

42 ocal adhesion kinase (FAK) and breast cancer anti-estrogen resistance 1 (BCAR1).

43 s study, we report that lncRNA breast cancer anti-estrogen resistance 4 (BCAR4) is required for YAP-d

44 30(cas) Src-binding domain (SBD) and induces anti-estrogen resistance in breast cancer cell lines as

45 The emergence of anti-estrogen resistance in breast cancer is an importan

46 tes acquisition of estrogen-independence and anti-estrogen resistance in vivo in breast cancer cells.

47 ted with tumor recurrence and development of anti-estrogen resistance.

48 2 promotion of breast cancer progression and anti-estrogen resistance.

49 However, anti-estrogen-resistant growth of ER-positive tumors rem

50 ERbeta mutants were seen in the estrogen and anti-estrogen responses at an AP-1 site.

51 ctive mRNA translational reprogramming to an anti-estrogen state by Runx2 and other mRNAs.

52 ER is the target for anti-estrogens such as tamoxifen (TAM).

53 Anti-estrogens such as tamoxifen inhibit the growth of E

54 Anti-estrogens, such as tamoxifen, have been used as the

55 In contrast, the anti-estrogen tamoxifen (TAM) recruits corepressors but

56 The non-steroidal anti-estrogen tamoxifen [TAM] has been in clinical use o

57 MCF7-Y537S cells were resistant to the anti-estrogen tamoxifen and fulvestrant.

58 ther the I3C dimerization product DIM or the anti-estrogen tamoxifen induced a G1 cell cycle arrest w

59 the resistance of breast cancer cells to the anti-estrogen tamoxifen.

60 established anti-tumor agents, including the anti-estrogens tamoxifen and faslodex.

61 differently in response to estradiol and the anti-estrogens tamoxifen and raloxifene.

62 Estradiol increased and anti-estrogens (tamoxifen and ICI 164,384) downregulated

63 The anti-estrogen, tamoxifen, increased pressure-induced con

64 tion without compromising sensitivity to the anti-estrogen, tamoxifen.

65 Tamoxifen (TAM), a nonsteroidal anti-estrogen that is widely used in chemotherapy, is kn

66 where ovarian function remains intact, these anti-estrogen therapies are not as effective.

67 binatorial trials of PFKFB3 antagonists with anti-estrogen therapies in ER(+) stage IV breast cancer

68 ive activity and continued responsiveness to anti-estrogen therapies in vitro.

69 tions for the development and application of anti-estrogen therapies to treat cancer in premenopausal

70 strogen receptor (ER(+)) and is treated with anti-estrogen therapies, particularly tamoxifen in preme

71 ha through PRL/PAK1 may impart resistance to anti-estrogen therapies.

72 However, anti-estrogen therapy has not been shown to be effective

73 cancers either does not initially respond to anti-estrogen therapy or develops resistance to such tre

74 Important new data on anti-estrogen therapy, including aromatase inhibitors an

75 cated in the development of insensitivity to anti-estrogen therapy.

76 breast cancer patients who are resistant to anti-estrogen therapy.

77 for breast cancer regression resulting from anti-estrogen therapy.

78 ed signaling, tumor growth and its effect on anti-estrogen therapy.

79 cancer contribute to acquired resistance to anti-estrogen therapy.

80 s prediction is tested using fulvestrant, an anti-estrogen too large to pass through the closed pore,

81 BIK is inducible by estrogen-starvation and anti-estrogen treatment and plays an important role in a