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1 ed with only 35% of the animals treated with toremifene.
2 acebo group, but not in animals treated with toremifene.
11 ive estrogen receptor modulators, tamoxifen, toremifene, and raloxifene with estradiol when given ora
12 ase in the protein melting temperature after toremifene binding, while ibuprofen has only a marginal
13 oxifen and most mice (12 of 14) treated with toremifene, but in none of the vehicle-dosed controls, i
15 biopsy were randomly assigned 1:1 to receive toremifene citrate 20 mg or placebo in a 3-year phase II
17 ene group (6.6 mg/kg/day); (b) the high-dose toremifene group (33 mg/kg/day); and (c) the control pla
18 gregated into three groups: (a) the low-dose toremifene group (6.6 mg/kg/day); (b) the high-dose tore
19 group (n = 10), at week 21 in the high-dose toremifene group (n = 12), and at week 29 in the low-dos
21 group and decreased by 8.1% +/- 1.4% in the toremifene group (P = .001 for between group comparison)
26 to the paucity of long-term clinical data on toremifene, important unresolved questions remain, which
30 0 men with biopsy-diagnosed HGPIN to receive toremifene or placebo for 3 years or until a diagnosis o
33 drogen receptor expression, the mechanism of toremifene's chemopreventive activity may be through non
35 n contrast, the dehalogenated TAM derivative toremifene (TOR) did not inhibit MM cell proliferation.
36 hronic administration of tamoxifen (TAM) and toremifene (TOR) on genetic damage related to carcinogen
37 nown to promote hepatocarcinoma in rats, but toremifene (TOR), a chlorinated TAM analogue, did not.
38 nhibitor (AI) atamestane (ATA) combined with toremifene (TOR; complete estrogen blockade) versus letr
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