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1 th a fluorescently labeled steroid analogue, estramustine.
2 (grade 1 to 2) nausea and fatigue related to estramustine.
3 ABC2 mRNA sensitized the resistant cells to estramustine.
4 e had no effect on direct labeling with [14C]estramustine.
5 lay a role in the response to the effects of estramustine.
6 1-hour infusions of 60 to 100 mg/m(2)), oral estramustine (10 mg/kg), and carboplatin (area under the
11 6.3 months in the group given docetaxel and estramustine and 3.2 months in the group given mitoxantr
12 , 338 were assigned to receive docetaxel and estramustine and 336 to receive mitoxantrone and prednis
15 nd doxorubicin alternating with vinblastine, estramustine, and androgen ablation followed by prostate
16 administration of docetaxel 70 mg/m(2), oral estramustine, and low-dose daily hydrocortisone in men w
21 f colchicine to tubulin was not inhibited by estramustine as detected by fluorescence and DEAE filter
22 ival of nearly two months with docetaxel and estramustine, as compared with mitoxantrone and predniso
24 , a variety of nonhormonal agents, including estramustine-based therapy, suramin, mitoxantrone, and d
25 doxorubicin alternating with vinblastine and estramustine before emergence of a castrate-resistant ph
28 t prostate cancer treated with docetaxel and estramustine (DE) or mitoxantrone and prednisone (MP).
30 Pharmacokinetics of EMP and the metabolites estramustine (EaM), estromustine (EoM), estradiol, and e
32 s indicated its role in cholesterol/steroid (estramustine, estradiol, and progesterone) trafficking/s
33 doxorubicin alternating with vinblastine and estramustine, given in addition to standard androgen dep
34 d the covalent labeling of tubulin with [14C]estramustine in a dose-dependent fashion and were noncom
37 c carcinoma cells, the incorporation of [14C]estramustine into the beta III isotype of tubulin was fo
38 ded phase II dose of docetaxel combined with estramustine is 70 mg/m2 in MPT patients and 60 mg/m2 in
39 ole/doxorubicin alternating with vinblastine/estramustine (KA/VE) or paclitaxel, estramustine, and or
40 axol, the antimitotic mechanism of action of estramustine may be due to kinetic stabilization of spin
41 bined suppressive effects of vinblastine and estramustine on the rate and extent of shortening and dy
43 ials have shown that docetaxel combined with estramustine or corticosteroids improves survival in met
44 y 2 weeks off, either alone or together with estramustine phosphate (EM-V) 600 mg/m(2) PO days 1 thro
48 on and overexpression of ABC2 contributes to estramustine resistance and provides the first indicatio
52 ty labeling of microtubule protein with [14C]estramustine resulted in the labeling of both alpha- and
54 However, by video microscopy, we find that estramustine strongly stabilizes growing and shortening
55 ommon among patients receiving docetaxel and estramustine than among those receiving mitoxantrone and
56 was longer in the group given docetaxel and estramustine than in the group given mitoxantrone and pr
57 ents, each given in 21-day cycles: 280 mg of estramustine three times daily on days 1 through 5, 60 m
60 served that the rate of efflux of dansylated estramustine was increased in SKEM compared with control
61 The interaction of the antimitotic agent estramustine with bovine microtubule proteins and purifi
63 for the benefit derived from combined use of estramustine with vinblastine or taxol, two other drugs
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