ライフサイエンスコーパス: exemestane

1 romatase inhibitors (anastrozole, letrozole, exemestane).

2 nt plus placebo, and 29 in those assigned to exemestane.

3 nd 3.4 months (3.0-4.6) in those assigned to exemestane.

4 231 to fulvestrant plus placebo, and 249 to exemestane.

5 values better than 1 nM, exceeding that for exemestane.

6 Only seven women were treated with exemestane.

7 e therapy after 2 to 3 years of tamoxifen to exemestane.

8 ch tumors may derive additional benefit from exemestane.

9 7 phase III trial comparing anastrozole with exemestane.

10 44% in the placebo group elected to receive exemestane.

11 mpared with a 7% increase from baseline with exemestane.

12 associated with either adjuvant tamoxifen or exemestane.

13 (HR) of 0.81 (95% CI, 0.72 to 0.92) favored exemestane.

14 as wild type from addition of everolimus to exemestane.

15 ombination with the aromatase inhibitor (AI) exemestane.

16 s no better than either fulvestrant alone or exemestane.

17 ose assigned to fulvestrant plus placebo and exemestane (0.95, 0.79-1.14; log-rank p=0.56).

18 e, 222 were reported as intercurrent deaths (exemestane, 107; tamoxifen, 115).

19 of -2.0 or more were accrued (147 allocated exemestane, 153 anastrozole); and 197 patients with base

20 ere detected after 8 hours of treatment with exemestane (200 nmol/L).

21 romatase inhibitor were randomly assigned to exemestane 25 mg daily plus entinostat 5 mg once per wee

22 e 1, patients received everolimus 10 mg plus exemestane 25 mg daily, with 10 mL of alcohol-free dexam

23 sive breast cancer were randomly assigned to exemestane 25 mg versus anastrozole 1 mg, daily.

24 e oral tamoxifen 20 mg/day or switch to oral exemestane 25 mg/day to complete a total of 5 years of a

25 g on days 15, 29, and every 28 days) or oral exemestane (25 mg once daily) on a 28-day cycle.

26 : Patients were randomized to treatment with exemestane (25 mg oral daily) together with everolimus (

27 , raloxifene (60 mg per day for 5 years) and exemestane (25 mg per day for 5 years) should also be di

28 60 postmenopausal women randomly assigned to exemestane (25 mg per day) compared with placebo in the

29 s anastrozole-matched placebo; or daily oral exemestane (25 mg).

30 moxifen were randomly assigned to 5 years of exemestane (25 mg/d orally) or 5 years of placebo.

31 In all, 930 BCFS events have been reported (exemestane, 423; tamoxifen, 507), giving an unadjusted h

32 disease-free survival had been reported (354 exemestane, 455 tamoxifen); unadjusted hazard ratio 0.76

33 Exemestane (6-methyleneandrosta-1,4-diene-3,17-dione) is

34 Aromatase inhibitors (AIs) such as exemestane, 6-methylideneandrosta-1,4-diene-3,17-dione,

35 ith baseline T-scores of less than -2.0 (101 exemestane, 96 anastrozole).

36 er two monthly treatments with goserelin and exemestane, a sensitive assay for serum estradiol was ch

37 Exemestane, a steroidal aromatase inhibitor, reduced inv

38 We postulated that exemestane-a mildly androgenic steroid-might have a less

39 76 (95% CI 0.66-0.88, p=0.0001) in favour of exemestane, absolute benefit 3.3% (95% CI 1.6-4.9) by en

40 exemestane and 2.8 months with placebo plus exemestane, according to assessments by local investigat

41 ficacy of this panel in the Tamoxifen versus Exemestane Adjuvant Multicenter (TEAM) trial.

42 The Tamoxifen and Exemestane Adjuvant Multinational (TEAM) trial included

43 r 5 years of median follow-up, the Tamoxifen Exemestane Adjuvant Multinational (TEAM) trial reported

44 participating in the international Tamoxifen Exemestane Adjuvant Multinational (TEAM) trial.

45 766 patients enrolled in the TEAM (Tamoxifen Exemestane Adjuvant Multinational) randomized clinical t

46 ree survival noted in patients who switch to exemestane after 2-3 years on tamoxifen persist after tr

47 romatase inhibitors may allow treatment with exemestane after a nonsteroidal aromatase inhibitor and

48 findings of the TEAM trial confirm that both exemestane alone and sequential treatment with tamoxifen

49 th the aromatase inhibitor exemestane versus exemestane alone.

50 Exemestane also inhibits the inflammatory increases in i

51 rcinoma in situ) breast cancers was 0.35% on exemestane and 0.77% on placebo (hazard ratio, 0.47; 95%

52 survival was 6.9 months with everolimus plus exemestane and 2.8 months with placebo plus exemestane,

53 ed; 72% in the exemestane group continued on exemestane and 44% in the placebo group elected to recei

54 llow-up of 4.1 years, 4-year EFS was 91% for exemestane and 91.2% for anastrozole (stratified hazard

55 ars did not differ significantly between the exemestane and anastrozole treatment groups (2.11%, 95%

56 parallel set of spectroscopic studies using exemestane and anastrozole.

57 received at least one dose of everolimus and exemestane and at least one confirmed dose of dexamethas

58 matitis in patients receiving everolimus and exemestane and could be a new standard of oral care for

59 breast cancers were detected in those given exemestane and in 32 of those given placebo, with a 65%

60 ibitor constant for the aromatase inhibitors exemestane and letrozole.

61 differ significantly between patients taking exemestane and patients taking anastrozole (-0.92%, 95%

62 and total hip between patients treated with exemestane and patients treated with anastrozole.

63 core predicts DRFS for patients treated with exemestane and patients treated with tamoxifen followed

64 we compared everolimus and exemestane versus exemestane and placebo (randomly assigned in a 2:1 ratio

65 Remarkably, combinations of exemestane and sulforaphane act highly synergistically,

66 onths, 162 (7%) and 115 (5%) patients in the exemestane and tamoxifen groups, respectively, had fract

67 exemestane; the absolute difference (between exemestane and tamoxifen) at 10 years in the population

68 responded to an absolute difference (between exemestane and tamoxifen) at 10 years of 4.0% (95% CI, 1

69 xifen, raloxifene, arzoxifene, lasofoxifene, exemestane, and anastrozole.

70 uential treatment with tamoxifen followed by exemestane are reasonable options as adjuvant endocrine

71 itors, including letrozole, anastrozole, and exemestane, are being incorporated into trials evaluatin

72 Overall, slightly more women in the exemestane arm (32%) than in the placebo arm (28%) disco

73 l (letrozole and anastrozole) and steroidal (exemestane) aromatase inhibitors may allow treatment wit

74 o evaluate the steroidal aromatase inhibitor exemestane as extended adjuvant therapy in this setting.

75 With 30 months of median follow-up, original exemestane assignment resulted in a borderline statistic

76 substantial proportion of patients, original exemestane assignment resulted in non-statistically sign

77 of AI treatment (anastrozole, letrozole, or exemestane), between August 1999 and June 2010 were retr

78 Within 6 months of switching to exemestane, BMD was lowered by 0.051 g/cm(3) (2.7%; 95%

79 s were aware of assignment to fulvestrant or exemestane, but not of assignment to anastrozole or plac

80 Despite premature closure and crossover to exemestane by a substantial proportion of patients, orig

81 The protective effect of switching to exemestane compared with continuing on tamoxifen on risk

82 s channel unoccupied in the enzyme-substrate/exemestane complexes.

83 d, placebo-controlled, double-blind trial of exemestane designed to detect a 65% relative reduction i

84 We have found that exemestane, different from letrozole and anastrozole, ca

85 ral tamoxifen (20 mg once a day) followed by exemestane for a total duration of 5 years.

86 ired for MCF-7Ca cells, whereas anastrozole, exemestane, formestane, and tamoxifen were ineffective a

87 Exemestane given for prevention has limited negative imp

88 f random assignment of treatment (19% of the exemestane group and 13% of the placebo group).

89 ed with 508 (22.1%) of 2,294 patients in the exemestane group and 603 (26.2%) of 2,305 patients in th

90 l at 10 years was 67% (95% CI 65-69) for the exemestane group and 67% (65-69) for the sequential grou

91 Adverse events occurred in 88% of the exemestane group and 85% of the placebo group (P=0.003),

92 follow-up, 921 (30%) of 3075 patients in the exemestane group and 929 (31%) of 3045 patients in the s

93 222 deaths occurred in the exemestane group compared with 261 deaths in the tamoxif

94 ients had been randomly assigned; 72% in the exemestane group continued on exemestane and 44% in the

95 val was demonstrated, with 352 deaths in the exemestane group versus 405 deaths in the tamoxifen grou

96 s were stomatitis (8% in the everolimus-plus-exemestane group vs. 1% in the placebo-plus-exemestane g

97 -exemestane group vs. 1% in the placebo-plus-exemestane group), anemia (6% vs. <1%), dyspnea (4% vs.

98 Exemestane had small negative effects on women's self-re

99 with baseline T-score of -2.0 or more taking exemestane had two fragility fractures and two other fra

100 Thus, exemestane has a wide range of previously unrecognized p

101 hibitors such as letrozole, anastrozole, and exemestane have proven to be effective endocrine regimen

102 Assignment to exemestane, having a smoking history, and current employ

103 tly shorter in patients randomly assigned to exemestane (hazard ratio [HR], 1.5; 95% CI, 1.1 to 2.1;

104 hat the on-treatment benefit of switching to exemestane (HR, 0.60; 95% CI, 0.48 to 0.75; P < .001) wa

105 The Society includes the aromatase inhibitor exemestane in addition to tamoxifen and raloxifene as a

106 east cancer patients treated with everolimus-exemestane in first and subsequent lines.

107 ree survival (PFS) when adding everolimus to exemestane in patients with advanced breast cancer exper

108 a sequential scheme of tamoxifen followed by exemestane in postmenopausal patients with early-stage,

109 (95% CI, 0.71 to 0.92; P = .001) in favor of exemestane in the ER-positive/ER unknown group.

110 mplying estrogen receptor (ER) dependence of exemestane-induced AREG expression.

111 Furthermore, exemestane-induced aromatase degradation can be complete

112 hanism that underlies exemestane resistance: exemestane induces AREG in an ER-dependent manner.

113 Exemestane induces aromatase degradation in a dose-respo

114 Because exemestane interacts with Asp(309) based on its co-cryst

115 patients treated with tamoxifen followed by exemestane irrespective of nodal status and chemotherapy

116 Exemestane is an active and well-tolerated third-line ho

117 A striking feature of the structure of exemestane is an extended system of conjugated Michael r

118 Entinostat added to exemestane is generally well tolerated and demonstrated

119 reast cancer prevention medication, although exemestane is not FDA approved for this indication.

120 The steroidal inhibitor exemestane is partially non-cross-resistant with nonster

121 rant plus placebo; eight in that assigned to exemestane), lethargy (three; 11; 11), and nausea or vom

122 nced breast cancer have examined the role of exemestane, letrozole, anastrozole, and fulvestrant in p

123 (block sizes 4-8) to either 5 years of oral exemestane monotherapy (25 mg once a day) or a sequentia

124 difference in disease-free survival between exemestane monotherapy and a sequential scheme of tamoxi

125 er taking fulvestrant (n = 45) compared with exemestane (n = 18; hazard ratio [HR], 0.52; 95% CI, 0.3

126 moxifen, were randomly assigned to switch to exemestane (n=2352) or to continue tamoxifen (n=2372) fo

127 One hundred sixteen patients (exemestane, n = 86; tamoxifen, n = 30; median age, 44 ye

128 The switch from tamoxifen to exemestane neither increased nor decreased endocrine sym

129 We also examined the effect of exemestane on aromatase mRNA level using real-time rever

130 The effect of exemestane on serum levels of estrogens and other steroi

131 d baseline T-scores of less than -2.0 taking exemestane, one had a fragility fracture and four had ot

132 ne of two adjuvant oral aromatase inhibitors-exemestane or anastrozole.

133 andomly assigned to switch from tamoxifen to exemestane or continue with tamoxifen until 5 years of t

134 Regardless of receiving exemestane or not, experiencing a worsening in any MENQO

135 re was 2.3% were randomly assigned to either exemestane or placebo.

136 to neoadjuvant AI therapy with anastrozole, exemestane, or letrozole.

137 freedom from breast cancer was 85.7% in the exemestane-ovarian suppression group (hazard ratio for r

138 re reported for 30.6% of the patients in the exemestane-ovarian suppression group and 29.4% of those

139 se-free survival at 5 years was 91.1% in the exemestane-ovarian suppression group and 87.3% in the ta

140 he two groups (hazard ratio for death in the exemestane-ovarian suppression group, 1.14; 95% CI, 0.86

141 om breast cancer at 5 years was 92.8% in the exemestane-ovarian suppression group, as compared with 8

142 sults indicate that the clinical benefits of exemestane over tamoxifen are achieved without significa

143 reased at all time points in women receiving exemestane (p<0.001).

144 domized, placebo-controlled trial evaluating exemestane, participants completed the Menopause-Specifi

145 samples from the Exemestane Versus Tamoxifen-Exemestane pathology study.

146 Exemestane patients reported more bone/muscle aches (P <

147 tries with MBC to exemestane plus placebo or exemestane plus everolimus.

148 OFS (95% CI, 64.0% to 84.4%), and 83.2% with exemestane plus OFS (95% CI, 72.7% to 90.0%).

149 t chemotherapy and were randomly assigned to exemestane plus OFS or tamoxifen plus OFS.

150 unmasked adjuvant treatment with 5 years of exemestane plus OFS or tamoxifen plus OFS.

151 ere is no strong indication to favour either exemestane plus OFS or tamoxifen plus OFS.

152 Patients on exemestane plus OFS reported more vaginal dryness, great

153 rticularly in the short term, in patients on exemestane plus OFS than patients on tamoxifen plus OFS.

154 mprovement of 10% to 15% in 5-year BCFI with exemestane plus OFS versus tamoxifen alone.

155 For TEXT patients, the benefit of exemestane plus OFS versus tamoxifen plus OFS in 5-year

156 mprovement of 5% or more in 5-year BCFI with exemestane plus OFS versus tamoxifen plus OFS or tamoxif

157 s and sweats over 5 years than were those on exemestane plus OFS, although these symptoms improved.

158 plus ovarian function suppression (OFS), or exemestane plus OFS.

159 OFS and 81.6% (95% CI, 69.8% to 89.2%) with exemestane plus OFS.

160 gnificant disease-free survival benefit with exemestane plus ovarian function suppression (OFS) compa

161 one receptor-positive breast cancer, testing exemestane plus ovarian function suppression (OFS), tamo

162 rly breast cancer to the aromatase inhibitor exemestane plus ovarian suppression or tamoxifen plus ov

163 early breast cancer, adjuvant treatment with exemestane plus ovarian suppression, as compared with ta

164 ifen, tamoxifen plus ovarian suppression, or exemestane plus ovarian suppression.

165 Further improvement was seen with the use of exemestane plus ovarian suppression.

166 y plus entinostat 5 mg once per week (EE) or exemestane plus placebo (EP).

167 from 189 centers in 24 countries with MBC to exemestane plus placebo or exemestane plus everolimus.

168 During the first year, most patients on exemestane plus triptorelin had E2 levels below the defi

169 ression method and were randomly assigned to exemestane plus triptorelin or tamoxifen plus triptoreli

170 Among patients on exemestane plus triptorelin, 25%, 24%, and 17% had an E2

171 With exemestane plus triptorelin, median reductions from base

172 g/mL at any time point during treatment with exemestane plus triptorelin.

173 cer, adjuvant OFS combined with tamoxifen or exemestane produces large improvements in BCFI compared

174 Our primary aim was to test whether exemestane prolongs disease-free survival (DFS).

175 propose a possible mechanism that underlies exemestane resistance: exemestane induces AREG in an ER-

176 Exemestane-resistant breast cancer cell lines (i.e., Exe

177 Exemestane should be considered another option as up-fro

178 Exemestane significantly reduced invasive breast cancers

179 of parental MCF-7aro cells with 1 micromol/L exemestane strongly induced the expression of AREG.

180 subgroup of women included in the Intergroup Exemestane Study (IES), a large randomised trial that co

181 Intergroup Exemestane Study (IES), an investigator-led study in 4,7

182 Conclusion The Intergroup Exemestane Study and contemporaneous studies have establ

183 Purpose The Intergroup Exemestane Study, an investigator-led study of 4,724 pos

184 rozole (T+LET R), anastrozole (T+ANA R), and exemestane (T+EXE R), as well as long-term estrogen depr

185 hat led to discontinuation of everolimus and exemestane (the most common were rash, hyperglycaemia, a

186 In the presence of 200 nmol/L exemestane, the t(1/2) of aromatase was reduced to 12.5

187 mprovement in overall survival was seen with exemestane; the absolute difference (between exemestane

188 moxifen were switched after 2.5-3.0 years to exemestane therapy for a total duration of 5.0 years of

189 l care for patients receiving everolimus and exemestane therapy.

190 assigned to continue tamoxifen or switch to exemestane to complete 5 years of adjuvant endocrine the

191 assigned to continue tamoxifen or switch to exemestane to complete a total of 5 years of adjuvant en

192 accrual to B-33, unblinding, and offering of exemestane to patients in the placebo group.

193 nhibitor everolimus may be administered with exemestane to postmenopausal women with MBC whose diseas

194 We show here that exemestane transcriptionally activates NAD(P)H:quinone o

195 We hypothesized that MA.27 anastrozole- or exemestane-treated patients with new or worsening vasomo

196 rols from the BOLERO-2 trial (everolimus and exemestane treatment in patients with hormone receptor-p

197 The impact of exemestane treatment on tumor-related signs and symptoms

198 We have found that exemestane treatment significantly reduces aromatase pro

199 In MA.27, anastrozole or exemestane treatment-emergent symptoms were not associat

200 rian Function Trial (SOFT) and Tamoxifen and Exemestane Trial (TEXT).

201 The TEXT (Tamoxifen and Exemestane Trial) and SOFT (Suppression of Ovarian Funct

202 nostat combined with the aromatase inhibitor exemestane versus exemestane alone.

203 randomized trial, we compared everolimus and exemestane versus exemestane and placebo (randomly assig

204 nt-by-marker effect for PgR was observed for exemestane versus tamoxifen (PgR-rich hazard ratio [HR],

205 Preferential exemestane versus tamoxifen treatment benefit was not pr

206 -fixed paraffin-embedded BC samples from the Exemestane Versus Tamoxifen-Exemestane pathology study.

207 R-positive) early breast cancer treated with exemestane versus tamoxifen.

208 Exemestane was administered at a dose of 25 mg/d orally

209 e therapy after 2 to 3 years of tamoxifen to exemestane was associated with clinically relevant impro

210 At 12 months, exemestane was associated with fewer hot flashes and les

211 During a median follow-up period of 3 years, exemestane was associated with no serious toxic effects

212 s) letrozole, anastrozole, and the steroidal exemestane were approved in the U.S. in the late 1990s f

213 The efficacy and safety of exemestane were clinically and radiographically evaluate

214 d hypercholesterolemia were less frequent on exemestane, whereas mild liver function abnormalities an

215 y a small excess number of women being given exemestane with clinically important worsening of QOL at

216 switch to the steroidal aromatase inhibitor exemestane with continuation of tamoxifen in the adjuvan

217 h or Without Arimidex) trial, which compared exemestane with fulvestrant-containing regimens in patie

218 sma from the SoFEA (Study of Faslodex Versus Exemestane With or Without Arimidex) trial, which compar