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1 eceptor-alpha (ERalpha) and are treated with anti-estrogens.
2 ing sensitivity to the inhibitory effects of anti-estrogens.
3 reased when administered in combination with anti-estrogens.
4 drugs representing three classes of clinical anti-estrogens.
5 rminants of the degree of resistance to some anti-estrogens.
6  to PI3K-mTORC1 blockers in combination with anti-estrogens.
7                                          The anti-estrogen 4-hydroxytamoxifen blocks Rsk2-mediated ac
8 , ER(+) cells also acquire resistance to the anti-estrogen 4-hydroxytamoxifen due to the rise of cycl
9 al estrogen receptors, as it is abrogated by anti-estrogen administration.
10 ffects of estrogen agonists and antagonists (anti-estrogens [AE]) on growth of MM cell lines and MM p
11            Endoxifen is known to be a potent anti-estrogen and its mechanisms of action are still bei
12 g domain is required for repression, because anti-estrogens and AF-2 mutations impair repression.
13 ted cell growth and synergized with approved anti-estrogens and cyclin-dependent kinase 4/6 inhibitor
14 ain (LBD), all of whom had been treated with anti-estrogens and estrogen deprivation therapies.
15  predictive of the clinical effectiveness of anti-estrogens and, as a result, downstream metabolic re
16 lective estrogen receptor modulators, a pure anti-estrogen, and genetic approaches impaired cancer ce
17                           The effects of the anti-estrogen, anion channel blocker, tamoxifen on amino
18 ailable on biphosphonates, ovarian ablation, anti-estrogens, anti-HER-2 (human epidermal growth facto
19                                              Anti-estrogens are a prime example of a targeted therapy
20                                        While anti-estrogens/aromatase inhibitors are initially effect
21 ly druggable because the C-terminal estrogen/anti-estrogen-binding domain is replaced with translocat
22 ive cell line as treatment of the cells with anti-estrogen-blocked cell death.
23 prostate-specific antigen was not blocked by anti-estrogens, but was blocked both by anti-androgens a
24 alpha, which in turn increases TAM-dependent anti-estrogen chemosensitivity in vitro and in vivo.
25 ls expressed estrogen receptors and the pure anti-estrogen compound, ICI 182780, did not induce apopt
26 ing resulted in decreased sensitivity to the anti-estrogen drug Tamoxifen but increased expression of
27 poptosis in response to staurosporine or the anti-estrogen drug tamoxifen.
28  cancer in these high-risk patients, such as anti-estrogen drugs and radical mastectomy, are limited
29 contact co-cultures; conferred resistance to anti-estrogen drugs; and enhanced tumor dissemination.
30        We hypothesized that a silicone based anti-estrogen-eluting implant placed within the breast w
31               Based on our recent finding of anti-estrogen/ER-beta-mediated growth inhibition of pros
32                                    Moreover, anti-estrogens frequently activate several signaling cas
33 for MED1 in mediating resistance to the pure anti-estrogen fulvestrant both in vitro and in vivo.
34                                         Pure anti-estrogen fulvestrant has been shown to be a promisi
35  for the ability to confer resistance to the anti-estrogen fulvestrant in 2 ER(+) breast cancer cell
36 uppression of migration was inhibited by the anti-estrogen ICI 164,384 and the gene transcription inh
37 eptor antagonist 4-Hydroxy-Tamoxifen and the anti-estrogen ICI 164383.
38 receptor alpha (ERalpha) and reversed by the anti-estrogen ICI 182, 780, and this response was not af
39 the inhibitory effects of treatment with the anti-estrogen ICI 182,780 on CXCR4-mediated tumor growth
40 CF-7 cells with the PFKFB3 inhibitor and the anti-estrogen ICI 182,780 synergistically induces apopto
41 kinase and MAPK activity, are blocked by the anti-estrogen ICI 182,780.
42 nists, estrogen, diethylstilbestrol, and the anti-estrogen ICI 182780 on cellular degradation of 3H-l
43 llowing ovariectomy or following exposure to anti-estrogen implanted directly into the gland.
44 tein expression is inducible by estrogen and anti-estrogens in ER-positive breast cancer cells.
45 bitors exhibit synergistic interactions with anti-estrogens in IntClust2 models.
46 gen treatment and plays an important role in anti-estrogen induced apoptosis of breast cancer cells.
47   Anti-pan-TGF-beta antibodies did not block anti-estrogen-induced recruitment in G1 and inhibition o
48 ynthesis of ERalpha and FOXM1 contributes to anti-estrogen insensitivity in ER(+) breast cancer.
49  the deregulation of FOXM1 may contribute to anti-estrogen insensitivity.
50 ogated the cell cycle arrest mediated by the anti-estrogen OHT.
51 her, effects of estrogens or highly specific anti-estrogens on bone turnover do not support the hypot
52  shown that estrogen inhibits Notch, whereas anti-estrogens or estrogen withdrawal activate Notch sig
53 ogens on early mesenchymal cell progenitors, anti-estrogen receptor-alpha (anti-ER alpha) Ab's stain
54                                      Because anti-estrogens reduced PTTG expression in human pituitar
55 ocal adhesion kinase (FAK) and breast cancer anti-estrogen resistance 1 (BCAR1).
56 s study, we report that lncRNA breast cancer anti-estrogen resistance 4 (BCAR4) is required for YAP-d
57 30(cas) Src-binding domain (SBD) and induces anti-estrogen resistance in breast cancer cell lines as
58                             The emergence of anti-estrogen resistance in breast cancer is an importan
59 tes acquisition of estrogen-independence and anti-estrogen resistance in vivo in breast cancer cells.
60 ted with tumor recurrence and development of anti-estrogen resistance.
61 2 promotion of breast cancer progression and anti-estrogen resistance.
62 3-mediated P-SMAD1/5 and p21 upregulation in anti-estrogen-resistant cells.
63                                     However, anti-estrogen-resistant growth of ER-positive tumors rem
64 ERbeta mutants were seen in the estrogen and anti-estrogen responses at an AP-1 site.
65 ctive mRNA translational reprogramming to an anti-estrogen state by Runx2 and other mRNAs.
66                         ER is the target for anti-estrogens such as tamoxifen (TAM).
67                                              Anti-estrogens such as tamoxifen inhibit the growth of E
68                                              Anti-estrogens, such as tamoxifen, have been used as the
69                             In contrast, the anti-estrogen tamoxifen (TAM) recruits corepressors but
70                            The non-steroidal anti-estrogen tamoxifen [TAM] has been in clinical use o
71       MCF7-Y537S cells were resistant to the anti-estrogen tamoxifen and fulvestrant.
72 ther the I3C dimerization product DIM or the anti-estrogen tamoxifen induced a G1 cell cycle arrest w
73 and ovaries or five years treatment with the anti-estrogen tamoxifen or aromatase inhibitors.
74 the resistance of breast cancer cells to the anti-estrogen tamoxifen.
75 established anti-tumor agents, including the anti-estrogens tamoxifen and faslodex.
76 differently in response to estradiol and the anti-estrogens tamoxifen and raloxifene.
77                      Estradiol increased and anti-estrogens (tamoxifen and ICI 164,384) downregulated
78                                          The anti-estrogen, tamoxifen, increased pressure-induced con
79 tion without compromising sensitivity to the anti-estrogen, tamoxifen.
80              Tamoxifen (TAM), a nonsteroidal anti-estrogen that is widely used in chemotherapy, is kn
81                                              Anti-estrogen therapies are available to prevent postmen
82 where ovarian function remains intact, these anti-estrogen therapies are not as effective.
83 binatorial trials of PFKFB3 antagonists with anti-estrogen therapies in ER(+) stage IV breast cancer
84 ive activity and continued responsiveness to anti-estrogen therapies in vitro.
85 tions for the development and application of anti-estrogen therapies to treat cancer in premenopausal
86 strogen receptor (ER(+)) and is treated with anti-estrogen therapies, particularly tamoxifen in preme
87 ha through PRL/PAK1 may impart resistance to anti-estrogen therapies.
88                                     However, anti-estrogen therapy has not been shown to be effective
89 cancers either does not initially respond to anti-estrogen therapy or develops resistance to such tre
90                        Important new data on anti-estrogen therapy, including aromatase inhibitors an
91 se outcome following adjuvant treatment with anti-estrogen therapy, independently of age, tumor grade
92  cancer contribute to acquired resistance to anti-estrogen therapy.
93 cated in the development of insensitivity to anti-estrogen therapy.
94  breast cancer patients who are resistant to anti-estrogen therapy.
95  for breast cancer regression resulting from anti-estrogen therapy.
96 ed signaling, tumor growth and its effect on anti-estrogen therapy.
97 s prediction is tested using fulvestrant, an anti-estrogen too large to pass through the closed pore,
98  BIK is inducible by estrogen-starvation and anti-estrogen treatment and plays an important role in a
99 e that underlies breast cancer resistance to anti-estrogen treatments.