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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
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
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
20 events were significantly increased with all SERMs (odds ratio 1.73, 95% CI 1.47-2.05; p<0.0001).
23 ng can discern fundamental differences among SERMs and provides insight into the distinct biologies o
25 ancer compared with both tamoxifen users and SERM nonusers, suggesting a role for raloxifene in endom
27 These results indicate that estrogens and SERMs exert tissue-specific effects by regulating unique
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
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
42 ether, our results suggest that differential SERM effects on corepressor binding can explain differen
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
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
50 association constants (Ka) were measured for SERMs using varying lipid compositions to examine how li
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
59 ifen, selective estrogen receptor modifiers [SERMs], diet, and exercise) likely to favorably influenc
61 EDC is a non-nuclear selective ER modulator (SERM) in vivo, and in mice, non-nuclear ER signaling pro
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
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
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
85 emonstrate that the selective ER modulators (SERMs) 4-hydroxytamoxifen (4HT) and raloxifene are able
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
90 ding selective estrogen receptor modulators (SERMs) and selective androgen receptor modulators (SARMs
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
100 Selective estrogen receptor modulators (SERMs) mimic estrogen action in certain tissues while op
104 Selective estrogen receptor modulators (SERMs) show differential effects upon ERalpha activation
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
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
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
123 Lasofoxifene and arzoxifene are two newer SERMs that have recently been demonstrated to improve bo
126 ermined the differential response of a novel SERM, SP500263, on estrogen receptor (ER) alpha and the
128 re demonstrates an unexpected consequence of SERM treatment, which could help further define the comp
130 LBD structure reveals an unexpected mode of SERM-mediated ER antagonism, in which the stability of E
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
140 nd in vivo and that the clinical efficacy of SERMs for the treatment of malignant gliomas could poten
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
148 263 represents a member of a novel series of SERMs that is structurally unrelated to SERMs currently
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
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
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
163 the antiestrogenic effect of this prototype SERM, we performed an analysis of the cofactors that int
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
172 n addition to statins, our screen found that SERMs, antifungals, and several antipsychotic medication
174 estrogen agonist (ethynyl estradiol) and the SERM raloxifene, 7-(R) was found to be a potent SERM tha
176 We therefore investigated the effects of the SERM raloxifene on isolated rabbit coronary arteries.
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
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
188 estrogen receptor (ER) ligand binding, this SERM family was shown to provide both a range of ERalpha
190 ast cancers may be specifically resistant to SERMs, whereas they may be less resistant to estrogen wi
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
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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