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1                                              SERM, used in treatment of breast cancer and osteoporosi
2                                              SERM-membrane interactions were probed under multiple pH
3                                              SERMs bind ER, alter receptor conformation, and facilita
4                                              SERMs may be preferable to estrogens given their efficac
5                                              SERMs reduced the cellular sphingosine and subsequently
6                                              SERMs, which interact with estrogen receptor-alpha and e
7  In this study, we compared the effects of a SERM (PSK3471) and 2 estrens (estren-alpha and estren-be
8                                    Perhaps a SERM used to prevent osteoporosis could simultaneously p
9  the contention that trioxifene represents a SERM with potential antimetastatic efficacy for the trea
10 ndings demonstrate for the first time that a SERM other than tamoxifen can induce glioma cell apoptos
11 eoadjuvant trials of hormonal therapy with a SERM (tamoxifen or idoxifene) or an aromatase inhibitor
12    Depending on their functional activities, SERMs could then be developed for a variety of clinical
13                       To identify additional SERMs, a method to classify compounds based on different
14 rther development in order to obtain dual AI/SERM agents for breast cancer treatment.
15 he antiestrogenic SERM activity of a dual AI/SERM could act synergistically with AI activity to enhan
16 ue the estrogenic SERM activity of a dual AI/SERM could attenuate the undesired effects stemming from
17 etion caused by the AI activity of a dual AI/SERM, while in breast cancer tissue the antiestrogenic S
18                                      For all SERMs, incidence of invasive oestrogen (ER)-positive bre
19 creases N-CoR binding in the presence of all SERMs blocks AF-1 activity.
20 events were significantly increased with all SERMs (odds ratio 1.73, 95% CI 1.47-2.05; p<0.0001).
21                                     Although SERM-exposed DC exhibited increased ability to internali
22                                     Although SERMs have been available for clinical use for 50 years,
23 ng can discern fundamental differences among SERMs and provides insight into the distinct biologies o
24 is benzothiophene derivative demonstrated an SERM profile in preclinical studies.
25 ancer compared with both tamoxifen users and SERM nonusers, suggesting a role for raloxifene in endom
26 se regulated by ERbeta in response to E2 and SERMs.
27    These results indicate that estrogens and SERMs exert tissue-specific effects by regulating unique
28              To understand how estrogens and SERMs exert tissue-specific effects, we performed microa
29 nt target genes in response to estrogens and SERMs.
30 ed increase in uterine weight, while another SERM, tamoxifen, increased uterine weight.
31 e in breast cancer tissue the antiestrogenic SERM activity of a dual AI/SERM could act synergisticall
32 zothiophene SERM, raloxifene, the benzopyran SERM, (S)-3-(4-hydroxyphenyl)-4-methyl-2-[4-[2-(1-piperi
33 -alpha ethinyl estradiol, the benzothiophene SERM, raloxifene, the benzopyran SERM, (S)-3-(4-hydroxyp
34 loped to generate a family of benzothiophene SERMs.
35 ity in vivo, and suggest that benzothiophene SERMs may exert estrogen-like beneficial effects on chol
36 rocedure is reported yielding benzothiophene SERMs wherein redox activity and ER affinity are modulat
37 SHG measurements of the interactions between SERMs and artificial cell membranes and independent obse
38 is incidental biological activity induced by SERMs could be a plausible mechanism as to their inhibit
39 on profiles after ER activation by different SERMs in MDA-MB-231 human breast cancer cells stably tra
40  were treated with estradiol, four different SERMs, and the pure antiestrogen ICI 182,780.
41 the basis of the known response to different SERMs.
42 ether, our results suggest that differential SERM effects on corepressor binding can explain differen
43              This suggests that differential SERM repression of AF-1 involves HDAC-dependent corepres
44 on of NF-kappaB activation markedly enhances SERM-induced apoptosis, suggesting a role for NF-kappaB
45 esis is that in normal tissue the estrogenic SERM activity of a dual AI/SERM could attenuate the unde
46 ogen action can no longer be used to explain SERM action at different sites around the body.
47  molecular mechanisms potentially explaining SERM resistance in ER-positive/PR-negative tumors have b
48  was renamed raloxifene and became the first SERM for the treatment and prevention of osteoporosis as
49                                          For SERMs, current evidence supports tamoxifen use for breas
50 association constants (Ka) were measured for SERMs using varying lipid compositions to examine how li
51 or NF-kappaB in protecting glioma cells from SERM-induced cytotoxicity.
52                                 Furthermore, SERMs did not induce the AF-1-mediated activity from the
53                 Whereas the first generation SERMs/SERDs were discovered in a serendipitous manner, t
54 3 is a member of a series of next-generation SERMs with functional selectivity toward ER-alpha and a
55 impact on the discovery of second generation SERMs, some of which are in late stage clinical developm
56 king density, and cholesterol content impact SERM-membrane interactions.
57 repressor binding can explain differences in SERM effects on ERalpha activity.
58 ional activity of other nuclear receptors in SERM-treated cells.
59 ifen, selective estrogen receptor modifiers [SERMs], diet, and exercise) likely to favorably influenc
60  the recognition of selective ER modulation (SERM) that created a new dimension in therapeutics.
61 EDC is a non-nuclear selective ER modulator (SERM) in vivo, and in mice, non-nuclear ER signaling pro
62 as estradiol and the selective ER modulator (SERM) tamoxifen promote p53 antagonism.
63 respond less well to selective ER modulator (SERM) therapy than ER-positive/PR-positive tumors.
64 f the selective estrogen receptor modulator (SERM) family, is widely used in the treatment of estroge
65     A selective estrogen receptor modulator (SERM) for the potential treatment of hot flushes is desc
66 novel selective estrogen receptor modulator (SERM) for the potential treatment of uterine leiomyoma i
67 is a Selective Estradiol Receptor Modulator (SERM) from soy.
68  of a selective estrogen receptor modulator (SERM) in the general population and characterize the end
69 f the selective estrogen receptor modulator (SERM) tamoxifen were synthesized and evaluated for their
70  of a selective estrogen receptor modulator (SERM) that has a dihydrobenzoxathiin core structure bear
71 ation selective estrogen receptor modulator (SERM) that has been approved for the prevention and trea
72  is a selective estrogen receptor modulator (SERM) that is a potent estrogen antagonist in mammary an
73  16), selective estrogen receptor modulator (SERM) therapy (n = 8), and no (hormone replacement) ther
74  is a selective estrogen receptor modulator (SERM) which is currently under clinical evaluation for t
75  is a selective estrogen receptor modulator (SERM) with competitive binding activity against estradio
76 en, a selective estrogen receptor modulator (SERM), represents the standard of care for many patients
77 ation selective estrogen receptor modulator (SERM), tamoxifen, and raloxifene side-by-side in in vitr
78 issue-selective estrogen receptor modulator (SERM), which acts as an antiestrogen in the mammary tiss
79 ation selective estrogen receptor modulator (SERM)-because this benzothiophene derivative demonstrate
80 issue-selective estrogen receptor modulator (SERM).
81 enous selective estrogen receptor modulator (SERM).
82 cause breast cancer selective ER modulators (SERM) are therapeutically ineffective in EOC, we suggest
83 utic selective estrogen receptor modulators (SERM), raloxifene and tamoxifen, can perturb DC developm
84 the selective oestrogen-receptor modulators (SERM).
85 emonstrate that the selective ER modulators (SERMs) 4-hydroxytamoxifen (4HT) and raloxifene are able
86 ring treatment with selective ER modulators (SERMs) such as tamoxifen.
87 Selective estrogen-receptor (ER) modulators (SERMs) are synthetic nonsteroidal compounds that switch
88 selective estrogen receptor (ER) modulators (SERMs) tamoxifen and raloxifene, cause antagonistic and
89  and selective estrogen receptor modulators (SERMs) activated the AF-2 mutants.
90 ding selective estrogen receptor modulators (SERMs) and selective androgen receptor modulators (SARMs
91 ding selective estrogen receptor modulators (SERMs) and/or aromatase inhibitors (AIs).
92      Selective Estrogen Receptor Modulators (SERMs) are a new class of drugsthat bind to estrogen rec
93      Selective estrogen receptor modulators (SERMs) demonstrate tissue-specific estrogen receptor (ER
94 s or selective estrogen receptor modulators (SERMs) has not been determined.
95      Selective estrogen receptor modulators (SERMs) have been defined as compounds that display tissu
96 y of selective estrogen receptor modulators (SERMs) have relied on ER binding and cell-based estrogen
97 t as selective estrogen receptor modulators (SERMs) in women, with estrogen-like activities on some p
98  and selective estrogen receptor modulators (SERMs) interact with estrogen receptor (ER) alpha and be
99 s of selective estrogen receptor modulators (SERMs) is thought to underlie their clinical use.
100      Selective estrogen receptor modulators (SERMs) mimic estrogen action in certain tissues while op
101  of selective oestrogen receptor modulators (SERMs) on breast cancer incidence.
102 t of selective estrogen receptor modulators (SERMs) on the brain.
103      Selective estrogen receptor modulators (SERMs) partially avoid such unwanted effects, but their
104      Selective estrogen receptor modulators (SERMs) show differential effects upon ERalpha activation
105      Selective estrogen receptor modulators (SERMs) such as tamoxifen are effective in the treatment
106 ther selective estrogen receptor modulators (SERMs) such as tamoxifen have estrogen-like effects in t
107  the Selective Estrogen Receptor Modulators (SERMs) tamoxifen and raloxifene, so called for their abi
108 n as selective estrogen receptor modulators (SERMs) that possess estrogen agonist-like actions on bon
109      Selective estrogen receptor modulators (SERMs) that suppress bone remodeling will change trabecu
110 n of selective estrogen receptor modulators (SERMs) with lipid membranes has been measured at clinica
111 gen, selective estrogen receptor modulators (SERMs), and bisphosphonates has been well described.
112 t of selective estrogen receptor modulators (SERMs), novel chromene scaffolds, benzopyranobenzoxapane
113 ding selective estrogen receptor modulators (SERMs), possess selective anti-Ebola activities.
114 lude selective estrogen receptor modulators (SERMs), prophylactic surgery, and lifestyle change.
115      Selective estrogen receptor modulators (SERMs), such as tamoxifen (4-OHT), bind to the ER and af
116 (AI)/selective estrogen receptor modulators (SERMs).
117 lled selective estrogen receptor modulators (SERMs).
118 y of selective estrogen receptor modulators (SERMs).
119 our selective oestrogen receptor modulators (SERMs; tamoxifen, raloxifene, arzoxifene, and lasofoxife
120 tor (selective estrogen receptor modulators (SERMs]); or (2) inhibit estrogen-synthesizing enzymes, t
121                                         Most SERMs are polyaromatic phenols susceptible to oxidative
122                                  Several new SERM agents are in clinical development in an attempt to
123    Lasofoxifene and arzoxifene are two newer SERMs that have recently been demonstrated to improve bo
124                                      A novel SERM (selective estrogen receptor modulators), 1-(R), a
125            These data identify 4c as a novel SERM with greater potency to antagonize estrogen in uter
126 ermined the differential response of a novel SERM, SP500263, on estrogen receptor (ER) alpha and the
127            Under active evaluation are novel SERMs, aromatase inhibitors/inactivators, gonadotrophin-
128 re demonstrates an unexpected consequence of SERM treatment, which could help further define the comp
129 l cancer prevention and individualization of SERM therapy.
130  LBD structure reveals an unexpected mode of SERM-mediated ER antagonism, in which the stability of E
131         DC differentiated in the presence of SERM were assessed for their capacity to internalize flu
132  antiestrogen-like (apoptosis) activities of SERMs on the basis of their gene expression profiles is
133 in, we demonstrated that the same dosages of SERMs which induced cholesterol accumulation also inhibi
134                                The effect of SERMs on the coronary vasculature is unknown.
135 verses the differential inhibitory effect of SERMs upon AF-1 activity in MCF-7 cells.
136 tored the growth-inhibitory effectiveness of SERMs in endocrine-resistant cells.
137             The therapeutic effectiveness of SERMs such as tamoxifen and raloxifene in breast cancer
138                                   Effects of SERMs on men with coronary artery disease (CAD) have not
139  propose a model for differential effects of SERMs on N-CoR binding.
140 nd in vivo and that the clinical efficacy of SERMs for the treatment of malignant gliomas could poten
141 data strongly support clinical evaluation of SERMs for the treatment of men with CAD.
142 in the development of the next generation of SERMs/SERDs, some of which are likely to have a major im
143 arified the specific anti-Ebola mechanism of SERMs, even the cationic amphiphilic drugs (CADs), this
144     The sometimes surprising pharmacology of SERMs has resulted in a growing interest in the developm
145 ach to improve the therapeutic properties of SERMs.
146 specific or represents a general property of SERMs is unknown.
147          Conversely, the redox reactivity of SERMs may contribute to antioxidant and chemopreventive
148 263 represents a member of a novel series of SERMs that is structurally unrelated to SERMs currently
149               By analyzing the structures of SERMs and their incidental biological activity (choleste
150 serum cholesterol values compared with older SERMs in smaller clinical trials.
151 er EFP values than did women receiving NT or SERM therapy (6.2 mL . 100 g(-1) . min(-1)+/- 2.4 and 5.
152 .1) (P = .012 and P = .008, respectively) or SERM therapy (3.9 mL . 100 g(-1) . min(-1)+/- 1.1) (P =
153 ticle by Spurgeon et al which evaluates oral SERM raloxifene as a potential therapeutic agent for HPV
154                                        Other SERMs are in development, with the goal of reducing toxi
155 ively elicited by tamoxifen but not by other SERMs, such as raloxifene or ICI182,780 (Fulvestrant).
156 ngs indicate that BZA is distinct from other SERMs in its ability to inhibit hormone-independent brea
157 terized the effects of BZA and several other SERMs on the proliferation of hormone-dependent MCF-7 an
158                    Tamoxifen, the pioneering SERM, blocks estrogen action by binding to the ER in bre
159 M raloxifene, 7-(R) was found to be a potent SERM that behaved as antagonist in the uterus and exhibi
160 pounds, LY357489,4, is among the most potent SERMs described to date with in vivo efficacy on bone an
161         To discover new classes of potential SERMs, we have employed a cell-free microsphere-based bi
162                                A promiscuous SERM ER complex creates a stimulatory signal in growth f
163  the antiestrogenic effect of this prototype SERM, we performed an analysis of the cofactors that int
164                   Raloxifene, a prototypical SERM, has ER agonist properties in bone and on cholester
165           These events cause drug-resistant, SERM-stimulated growth.
166  centers in the monkey, suggesting that some SERMs may share estrogen's neuroprotective potential for
167 e developed an in vitro system in which some SERMs (4-hydroxytamoxifen and resveratrol) demonstrate e
168 able, with some (bisphosphonates, tamoxifen, SERMs, and exercise) likely to favorably influence breas
169  pharmacologic discovery of ovarian-targeted SERM.
170                     These results imply that SERM activity is dependent on a conformational change of
171              These observations suggest that SERM may depress immunity when given to healthy individu
172 n addition to statins, our screen found that SERMs, antifungals, and several antipsychotic medication
173         Recent clinical trials indicate that SERMs are useful in treatment of disorders of bone and m
174 estrogen agonist (ethynyl estradiol) and the SERM raloxifene, 7-(R) was found to be a potent SERM tha
175  in vivo biological assays reflective of the SERM profile.
176 We therefore investigated the effects of the SERM raloxifene on isolated rabbit coronary arteries.
177  no effect on the potency or efficacy of the SERM raloxifene.
178    Furthermore, the selective ability of the SERM tamoxifen but not raloxifene to regulate miR-451 an
179 l (BCPT) demonstrated the superiority of the SERM tamoxifen to placebo in reducing breast cancer risk
180  higher concentrations than estradiol or the SERM, and acted for the most part through the AR.
181                                          The SERMs investigated in this study include raloxifene, tam
182 is of gene stimulation and inhibition by the SERMs trans-hydroxytamoxifen (TOT) and raloxifene (Ral)
183 embranes and independent observations of the SERMs efficacy from clinical studies suggests that quant
184                     We found that all of the SERMs inhibited the growth of MCF-7, T47D, and MCF-7:2A
185                           In addition to the SERMs, however, have emerged the Selective Estrogen Degr
186                               Theoretically, SERMs could be synthesized that would exhibit nearly com
187          This phenotype indicates that these SERM act to maintain DC in an immature state by inhibiti
188  estrogen receptor (ER) ligand binding, this SERM family was shown to provide both a range of ERalpha
189 ic capsules concurrently with the last three SERM injections (immediate, group 1).
190 ast cancers may be specifically resistant to SERMs, whereas they may be less resistant to estrogen wi
191 cruitment determine the cellular response to SERMs.
192 s of SERMs that is structurally unrelated to SERMs currently on the market or in clinical development
193 ng efficacy as well as toxicity of these two SERMs in a similar high-risk population, will be availab
194                                 Of these two SERMs, raloxifene is preferred because it has markedly l
195 roperties may be important for understanding SERM action in vivo.
196                                       Unlike SERMs, the estrens induced reproductive organ hypertroph
197 ng the average length of the cracks, whereas SERM treatments lead to a more ductile fracture and main
198 ifen and CC-8490, a novel benzopyranone with SERM activity, induce glioma cell apoptosis in a dose- a

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