ライフサイエンスコーパス: aromatase inhibitor

1 in-releasing hormone agonist/antagonist plus aromatase inhibitor.

2 be administered with either tamoxifen or an aromatase inhibitor.

3 a diagnosis of MBC and prior exposure to an aromatase inhibitor.

4 , but only eight individuals had received an aromatase inhibitor.

5 at had been treated with letrozole, a potent aromatase inhibitor.

6 rs clinically responsive and resistant to an aromatase inhibitor.

7 r more prescriptions for tamoxifen and/or an aromatase inhibitor.

8 ers that have progressed on tamoxifen and/or aromatase inhibitors.

9 ET, evenly distributed between tamoxifen or aromatase inhibitors.

10 ed by adjuvant therapy with antiestrogens or aromatase inhibitors.

11 signed and synthesized as nonsteroidal CYP19 aromatase inhibitors.

12 he development of new pyrroloquinoline-based aromatase inhibitors.

13 dicted the treatment outcomes for first-line aromatase inhibitors.

14 cancer previously treated with nonsteroidal aromatase inhibitors.

15 pallium) cytoarchitecture in the presence of aromatase inhibitors.

16 dict interpatient variability in response to aromatase inhibitors.

17 ry the response of breast cancer patients to aromatase inhibitors.

18 l lacking in pediatric patients treated with aromatase inhibitors.

19 uated prospectively in patients treated with aromatase inhibitors.

20 m can be used for developing next-generation aromatase inhibitors.

21 d 1 analogues that were evaluated as QR2 and aromatase inhibitors.

22 ures to millions of potential mixtures of 86 aromatase inhibitors.

23 st cancer, and confer clinical resistance to aromatase inhibitors.

24 mutations associate with a lower response to aromatase inhibitors.

25 per se may counteract the intended effect of aromatase inhibitors.

26 Treatment with the aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD

27 which occur in 25-30% of people treated with aromatase inhibitors(1)(-4), knowledge about clinical re

28 positron emission tomography (PET) with the aromatase inhibitor [(11)C]vorozole in a sample of 43 ad

29 or plus a CDKI, 932 received placebo plus an aromatase inhibitor, 1296 received fulvestrant plus a CD

30 versus C-7 allyl derivatives led to the best aromatase inhibitor 13 of this work with IC(50) of 0.055

31 least one prescription for tamoxifen (43%), aromatase inhibitors (26%), or both (30%) within 1 year

32 ine therapy compared with a third-generation aromatase inhibitor, a standard of care for first-line t

33 ced breast cancer and acquired resistance to aromatase inhibitors, a daily dose of 6 mg of estradiol

34 ity to cancer cells, whereas letrozole is an aromatase inhibitor administered after surgery to post-m

35 tablished that a strategy of switching to an aromatase inhibitor after 2 to 3 years of tamoxifen can

36 ast cancers, which confers resistance to the aromatase inhibitor (AI) anastrozole (Ana) when expresse

37 adjuvant treatment strategy incorporating an aromatase inhibitor (AI) as primary (initial endocrine t

38 n suppression (OFS), in combination with the aromatase inhibitor (AI) exemestane.

39 d breast cancer or MBC were treated with the aromatase inhibitor (AI) letrozole (2.5 mg orally daily)

40 s treatment would restore sensitivity to the aromatase inhibitor (AI) letrozole.

41 stigated adaptive mechanisms associated with aromatase inhibitor (AI) resistance in breast cancer cel

42 Purpose Adherence to aromatase inhibitor (AI) therapy for early-stage breast

43 ictive for progression-free survival time to aromatase inhibitor (AI) therapy in advanced breast canc

44 ESR1 mutations are selected by prior aromatase inhibitor (AI) therapy in advanced breast canc

45 ESR1 have been associated with resistance to aromatase inhibitor (AI) therapy in patients with ER+ me

46 tive study assessed the impact of 2 years of aromatase inhibitor (AI) therapy on the incidence of ova

47 m endocrine therapy but later progression on aromatase inhibitor (AI) therapy were given vorinostat (

48 c breast cancers (MBC) resistant to adjuvant aromatase inhibitor (AI) therapy.

49 ng recurrence/progression after nonsteroidal aromatase inhibitor (AI) therapy.

50 was > 10% after 2 to 4 weeks of neoadjuvant aromatase inhibitor (AI) therapy.

51 Preoperative aromatase inhibitor (AI) treatment promotes breast-conse

52 nformation exists on the long-term effect of aromatase inhibitor (AI) use on CVD risk in breast cance

53 Aromatase inhibitor (AI) use results in low estrogen lev

54 pendent kinase 4/6 (CDK4/6) inhibitor and an aromatase inhibitor (AI), given US Food and Drug Adminis

55 henotypes evolving in lines resistant to the aromatase inhibitor (AI).

56 The long-range goal has been to create dual aromatase inhibitor (AI)/selective estrogen receptor mod

57 Aromatase inhibitors (AI) are a standard-of-care treatme

58 Aromatase inhibitors (AI) are associated with significan

59 critical enzyme in estrogen biosynthesis and aromatase inhibitors (AI) are employed widely for endocr

60 Aromatase inhibitors (AI) are rapidly becoming the first

61 Aromatase inhibitors (AI) have become the first-line end

62 Aromatase inhibitors (AI) induce painful musculoskeletal

63 domain undergoes epigenetic reprogramming in aromatase inhibitors (AI)-resistant cells, leading to Ke

64 ER)+ post-menopausal breast cancer tumors to aromatase inhibitors (AI).

65 variables among three patient groups (no ET, aromatase inhibitor [AI], or tamoxifen) were compared by

66 ptoms are the most common adverse effects of aromatase inhibitors (AIs) and can result in decreased q

67 The association between use of aromatase inhibitors (AIs) and cardiovascular outcomes i

68 50% of breast cancer survivors treated with aromatase inhibitors (AIs) and is the most common reason

69 Aromatase inhibitors (AIs) are effective for treatment o

70 Although third-generation aromatase inhibitors (AIs) are important drugs in hormon

71 For postmenopausal women, aromatase inhibitors (AIs) are the preferred first-line

72 Aromatase inhibitors (AIs) are the standard endocrine th

73 omise quality of life.SIGNIFICANCE STATEMENT Aromatase inhibitors (AIs) are used as an adjuvant thera

74 Breast cancer patients using aromatase inhibitors (AIs) as an adjuvant therapy often

75 gen receptor-positive (ER+) breast cancer to aromatase inhibitors (AIs) but have been limited to smal

76 reported in randomized clinical trials with aromatase inhibitors (AIs) compared with tamoxifen.

77 Nonadherence to aromatase inhibitors (AIs) for breast cancer is common a

78 dverse events (MS-AEs) in women treated with aromatase inhibitors (AIs) for early breast cancer.

79 omen older than age 50 years who were taking aromatase inhibitors (AIs) for resected breast cancer wi

80 Aromatase inhibitors (AIs) have an established role in t

81 mergent symptoms with adjuvant tamoxifen and aromatase inhibitors (AIs) have been associated with sup

82 Aromatase inhibitors (AIs) increase the risk of osteopor

83 The so-called third generation aromatase inhibitors (AIs) letrozole, anastrozole, and t

84 E Women with breast cancer (BC) treated with aromatase inhibitors (AIs) may experience joint symptoms

85 Aromatase inhibitors (AIs) prevent estrogen production a

86 that therapy including tamoxifen citrate and aromatase inhibitors (AIs) reduces CBC risk.

87 Aromatase inhibitors (AIs) such as exemestane, 6-methyli

88 Adherence to tamoxifen, aromatase inhibitors (AIs), and overall AET (tamoxifen o

89 positive breast cancers initially respond to aromatase inhibitors (AIs), but eventually acquire resis

90 tamoxifen in patients with mBC resistant to aromatase inhibitors (AIs).

91 estrogen receptor modulators (SERMs) and/or aromatase inhibitors (AIs).

92 inhibited by the ER antagonist tamoxifen and aromatase inhibitor anastrazole and were increased by th

93 d from obese women reduce sensitivity to the aromatase inhibitor anastrazole in an organotypic breast

94 are lean or obese influence response to the aromatase inhibitor (anastrazole), we incorporated patie

95 RATIONALE: The aromatase inhibitor anastrozole blocks the conversion of

96 We assessed the efficacy and safety of the aromatase inhibitor anastrozole for prevention of breast

97 In these donors, exposure to the aromatase inhibitor anastrozole inhibited E2 production.

98 The aromatase inhibitor anastrozole inhibits estrogen synthe

99 ho had been randomly assigned to receive the aromatase inhibitor anastrozole plus the selective estro

100 n tissue samples, whereas when combined with aromatase inhibitor anastrozole significantly increased

101 therapy involves 5 years of the nonsteroidal aromatase inhibitors anastrozole and letrozole.

102 tagonist (fulvestrant); TES supplementation; aromatase inhibitor (anastrozole); and TES plus anastroz

103 nous estrogen in males and females using the aromatase inhibitor, anastrozole, in two models of PH: t

104 e the surprising discovery that one of these aromatase inhibitors, anastrozole, significantly increas

105 We analysed patients according to which aromatase inhibitor and T-score groups they were allocat

106 The association between aromatase inhibitors and cardiovascular outcomes among w

107 tially non-cross-resistant with nonsteroidal aromatase inhibitors and is a mild androgen and could pr

108 enopausal women with breast cancer receiving aromatase inhibitors, and can be administered without ad

109 Mammography, chemotherapy, tamoxifen, aromatase inhibitors, and trastuzumab.

110 d of estradiol, an ER agonist; letrozole, an aromatase inhibitor; and fulvestrant, a pure ER antagoni

111 estrogenemia may be treated efficiently with aromatase inhibitors; any change in appearance should pr

112 lthough s.c. treatment with testosterone and aromatase inhibitor applied beginning on the day of immu

113 Aromatase inhibitors are a standard of care for hormone

114 en and raloxifene and adequate evidence that aromatase inhibitors are associated with small to modera

115 Purpose Aromatase inhibitors are established breast cancer chemo

116 Aromatase inhibitors are important drugs to treat estrog

117 While anti-estrogens/aromatase inhibitors are initially effective, resistance

118 Third-generation aromatase inhibitors are more effective than tamoxifen f

119 Aromatase inhibitors are the mainstay of hormonal therap

120 Introduction: Aromatase inhibitors are the mainstay of hormonal therap

121 Aromatase inhibitors are the major first-line treatment

122 Aromatase inhibitors are the preferred treatment for cer

123 tment in cancer and other disorders in which aromatase inhibitors are useful.

124 h selective estrogen receptor modulators and aromatase inhibitors are widely used for the treatment o

125 Aromatase inhibitors are widely used in breast cancer an

126 adiol-sensitive disease were re-treated with aromatase inhibitors at estradiol progression, among whi

127 ubation of follicle-enclosed oocytes with an aromatase inhibitor, ATD, and enzymatic and manual remov

128 roves disease-free survival after 5 years of aromatase inhibitor-based therapy in women with postmeno

129 After 5 years of aromatase inhibitor-based therapy, 5 years of letrozole

130 ns on telomerase function, and letrozole, an aromatase inhibitor, blocked androgen effects on telomer

131 lets, exposure to 5alpha-R inhibitors or the aromatase inhibitor both inhibited T enhancement of GSIS

132 important in optimizing the clinical use of aromatase inhibitors, both in terms of identifying respo

133 docrine therapy, or who were treated with an aromatase inhibitor but who had received previous chemot

134 evels reported in postmenopausal patients on aromatase inhibitors, but at each time point, at least 1

135 n failure, androgen deprivation therapy, and aromatase inhibitors can all promote bone loss.

136 lts demonstrate that adjuvant treatment with aromatase inhibitors can be considered for breast cancer

137 Surgery is rarely indicated and aromatase inhibitors constitute an effective treatment f

138 rons under oxidative stress conditions in an aromatase inhibitor-dependent manner.

139 with advanced BC after resistance to TAM and aromatase inhibitors develops.

140 ver, pretreatment with fadrozole, a specific aromatase inhibitor, did not block norepinephrine's neur

141 eliminated or reduced by the addition of an aromatase inhibitor during CM generation.

142 Aromatase inhibitors effectively prevent breast cancer r

143 The Society includes the aromatase inhibitor exemestane in addition to tamoxifen

144 receptor-positive early breast cancer to the aromatase inhibitor exemestane plus ovarian suppression

145 study evaluated entinostat combined with the aromatase inhibitor exemestane versus exemestane alone.

146 0.24-0.80]; 2 trials [n = 17 806]), and the aromatase inhibitors exemestane and anastrozole (RR, 0.4

147 er were assigned to one of two adjuvant oral aromatase inhibitors-exemestane or anastrozole.

148 ased on experiments with FHMs exposed to the aromatase inhibitor fadrozole, we also show how a toxic

149 gyrus was assessed by local infusion of the aromatase inhibitor fadrozole, whose efficacy was confir

150 AvodartTM); (d) T + Letrozole (nonsteroidal aromatase inhibitor; FemeraTM); (e) Flutamide + ATD (and

151 Use of aromatase inhibitors, fenretinide, or other selective es

152 e of continuing tamoxifen or switching to an aromatase inhibitor for 10 years total adjuvant endocrin

153 Treatment with an aromatase inhibitor for 5 years as up-front monotherapy

154 e CDK4/6 inhibitor palbociclib combined with aromatase inhibitors for the treatment of estrogen recep

155 estosterone, neonatal males administered the aromatase inhibitor formestane exhibited dramatic change

156 e cyclooxygenase inhibitor nimesulide or the aromatase inhibitor formestane.

157 14.9 months (14.0-16.7) in the placebo plus aromatase inhibitor group (difference 13.1 months; range

158 n progression-free survival in the CDKI plus aromatase inhibitor group was 28.0 months (95% CI 25.3-2

159 nation chemotherapy, NET as monotherapy with aromatase inhibitors had a similar clinical response rat

160 Estrogen deprivation therapy with aromatase inhibitors has been hypothesized to paradoxica

161 However, development of resistance to aromatase inhibitors has been observed.

162 Blocking estrogen biosynthesis by aromatase inhibitors has therefore become a first-line e

163 Aromatase inhibitors have been reported to increase heig

164 Third-generation aromatase inhibitors have been widely used in postmenopa

165 and switching therapy between tamoxifen and aromatase inhibitors (HR, 1.50; 95% CI, 1.23 to 1.83) du

166 Although aromatase inhibitors improve disease-free survival, tamo

167 d adjuvant therapy with tamoxifen or with an aromatase inhibitor improved disease-free survival and i

168 Everolimus combined with an aromatase inhibitor improved progression-free survival i

169 Adjuvant therapy with an aromatase inhibitor improves outcomes, as compared with

170 DK4/6(i) palbociclib, in combination with an aromatase inhibitor in primary tumors.

171 breast cancer resistant to treatment with an aromatase inhibitor in the adjuvant or metastatic settin

172 ceiving previous therapy with a nonsteroidal aromatase inhibitor in the adjuvant setting or to treat

173 Third-generation aromatase inhibitors in combination with antiandrogens a

174 s to profile the effects on P450 activity of aromatase inhibitors in current clinical use for the tre

175 he optimal duration of extended therapy with aromatase inhibitors in patients with postmenopausal bre

176 ce 2008 regarding the safety and efficacy of aromatase inhibitors in pediatric patients.

177 needed to demonstrate safety and efficacy of aromatase inhibitors in pediatric patients.

178 matase inhibitor or tamoxifen followed by an aromatase inhibitor (in sequence).

179 dications, such as tamoxifen, raloxifene, or aromatase inhibitors, in women who are not at increased

180 omen with the polycystic ovary syndrome, but aromatase inhibitors, including letrozole, might result

181 Ralpha modulator drugs such as tamoxifen and aromatase inhibitors ineffective.

182 qAOP to predict effects of another, untested aromatase inhibitor, iprodione.

183 sitive disease, antiestrogen therapy with an aromatase inhibitor is a reasonable alternative to obser

184 to endocrine therapies such as tamoxifen and aromatase inhibitors is a significant clinical problem.

185 Treatment of breast cancer with aromatase inhibitors is associated with damage to bones.

186 Aromatase inhibitors lead to profound estrogen suppressi

187 n deprivation (LTED) with tamoxifen (TAM) or aromatase inhibitors leads to endocrine-resistance, wher

188 ighly proliferative after treatment with the aromatase inhibitor letrozole and identified a D189Y mut

189 rmal growth factor receptor 2 (HER2), to the aromatase inhibitor letrozole as first-line treatment of

190 R(+) breast cancers after treatment with the aromatase inhibitor letrozole.

191 ter pretreatment with a clinical dose of the aromatase inhibitor letrozole.

192 f CDKI or placebo with endocrine therapy (an aromatase inhibitor [letrozole or anastrazole] or fulves

193 mpletely abolished by pre-treatment with the aromatase inhibitor, letrozole.

194 attenuated by systemic administration of the aromatase inhibitor, letrozole.

195 he initial 5 years of follow-up after use of aromatase inhibitors (MAP.3 and International Breast Can

196 res and suggest that acute administration of aromatase inhibitors may be an effective treatment for S

197 disease pathogenesis in females and suggests aromatase inhibitors may have therapeutic potential.

198 Aromatase inhibitors might be more efficacious, and resu

199 s during which progression occurred included aromatase inhibitor (n = 36), fulvestrant (n = 21), and

200 rom their first prescription of tamoxifen or aromatase inhibitors (N = 3,395).

201 led before and after 4 months of neoadjuvant aromatase inhibitor (NAI) treatment.

202 ove 10% inhibition of estradiol synthesis by aromatase inhibitors, noticeable (eventually reversible)

203 cancer that has progressed on non-steroidal aromatase inhibitors (NSAIs) is unclear.

204 e of potential effects of random mixtures of aromatase inhibitors on the dynamics of women's menstrua

205 ified by type of previous endocrine therapy (aromatase inhibitors only vs selective oestrogen recepto

206 om 17 922 initiated treatment with either an aromatase inhibitor or tamoxifen (8139 and 9783, respect

207 nimum of 5 years of adjuvant therapy with an aromatase inhibitor or tamoxifen followed by an aromatas

208 ree after about 5 years of treatment with an aromatase inhibitor or tamoxifen followed by an aromatas

209 ther by blocking estrogen production through aromatase inhibitors or antiestrogens that compete for h

210 east cancer initiating hormonal therapy with aromatase inhibitors or tamoxifen between April 1, 1998,

211 de + ATD (androgen antagonist plus steroidal aromatase inhibitor); or (f) dihydrotestosterone (DHT) +

212 Birds were injected with fadrozole, a potent aromatase inhibitor, or vehicle within 2-5 minutes after

213 Aromatase inhibitors play a prominent role in the manage

214 he pooled analysis, of whom 1320 received an aromatase inhibitor plus a CDKI, 932 received placebo pl

215 Preoperative and perioperative aromatase inhibitor (POAI) therapy has the potential to

216 Aromatase inhibitors prevent breast cancer in postmenopa

217 Aromatase inhibitors prevent more contralateral breast c

218 lmethylflavones previously reported by us as aromatase inhibitors proved to be able to interact with

219 ucing medications (tamoxifen, raloxifene, or aromatase inhibitors) provide at least a moderate benefi

220 Exemestane, a steroidal aromatase inhibitor, reduced invasive breast cancer inci

221 ain adverse events were arthralgia and other aromatase-inhibitor related symptoms; no additional toxi

222 suggests that women with obesity experience aromatase inhibitor resistance at higher rates.

223 eutic target to combat or delay the onset of aromatase inhibitor resistance in breast cancer.

224 estrogen treatment of patients with acquired aromatase inhibitor resistance in clinical trials.

225 substantial improvements in patient outcome, aromatase inhibitor resistance remains a major clinical

226 nce of PIK3CA mutation, primary or secondary aromatase inhibitor resistance, and measurable or non-me

227 non-measurable disease, primary or secondary aromatase inhibitor resistance, PIK3CA status, and PTEN

228 ated RET signaling is enhanced in a model of aromatase inhibitor resistance.

229 antihormonal therapies such as tamoxifen and aromatase inhibitors, resistance often emerges.

230 d progression-free survival in patients with aromatase inhibitor-resistant advanced breast cancer.

231 ibitors may be an effective therapy to treat aromatase inhibitor-resistant breast cancers and that im

232 anamycin (17-DMAG) can inhibit the growth of aromatase inhibitor-resistant breast cancers and the mec

233 GDNF-RET signaling promoted the survival of aromatase inhibitor-resistant cells and elicited resista

234 has been approved for advanced or metastatic aromatase inhibitor-resistant ER(+) breast cancer.

235 Aromatase inhibitor-responsive MCF-7aro and aromatase inhibitor-resistant LTEDaro breast epithelial

236 ication of activating ESR1 gene mutations in aromatase inhibitor-resistant metastatic breast cancers.

237 xpression levels in an independent cohort of aromatase inhibitor-resistant patient specimens.

238 njection of estrogen receptor antagonists or aromatase inhibitors, respectively, decreases sexual mot

239 Aromatase inhibitor-responsive MCF-7aro and aromatase in

240 RR, 0.44 [95% CI, 0.24-0.80]; 2 trials), and aromatase inhibitors (RR, 0.45 [95% CI, 0.26-0.70]; 2 tr

241 r-resistant cells and elicited resistance in aromatase inhibitor-sensitive cells.

242 isk of cardiovascular events associated with aromatase inhibitors should be balanced with their favor

243 son of steroidal and nonsteroidal classes of aromatase inhibitors showed neither to be superior in te

244 ubing containing testosterone (T), T plus an aromatase inhibitor (T+ADT), or 5alpha-dihydrotestostero

245 reast cancer who had developed resistance to aromatase inhibitors, tamoxifen or fulvestrant.

246 of overall survival was not higher with the aromatase inhibitor than with placebo.

247 Letrozole is an aromatase inhibitor that has an unapproved use for ovula

248 Therapies targeting ER function, including aromatase inhibitors that block the production of estrog

249 estrogen receptor modulator tamoxifen and to aromatase inhibitors that lower circulating estradiol oc

250 s following failure of previous tamoxifen or aromatase inhibitor therapies.

251 from patients in two studies of neoadjuvant aromatase inhibitor therapy by massively parallel sequen

252 Adjuvant aromatase inhibitor therapy is well established in postm

253 rtant to understand the effects of long-term aromatase inhibitor therapy on BMD.

254 nd low bone mass who were receiving adjuvant aromatase inhibitor therapy, twice-yearly administration

255 otherapy, the interval from the last dose of aromatase-inhibitor therapy, and the duration of treatme

256 Aromatase inhibitors therefore constitute a frontline th

257 Extending treatment with an aromatase inhibitor to 10 years may further reduce the r

258 The extension of treatment with an adjuvant aromatase inhibitor to 10 years resulted in significantl

259 ree thermal regimes; some eggs were given an aromatase inhibitor to produce sons at temperatures that

260 as E2 release, and (3) direct infusion of an aromatase inhibitor to the S-ME suppressed spontaneous G

261 carcinogenesis and implicate superiority of aromatase inhibitors to antiestrogens for breast cancer

262 carcinogenesis and implicate superiority of aromatase inhibitors to antiestrogens for breast cancer

263 se of other selective ER modulators or other aromatase inhibitors to lower BC risk is not recommended

264 The application of aromatase inhibitors to postmenopausal breast cancer pat

265 enefits of taking tamoxifen, raloxifene, and aromatase inhibitors to reduce risk for breast cancer ar

266 n of combinations of histone deacetylase and aromatase inhibitors to treat ER-negative and endocrine-

267 Administration of letrozole, a specific aromatase inhibitor, to these mice blocked the stromal d

268 dications, such as tamoxifen, raloxifene, or aromatase inhibitors, to women who are at increased risk

269 Aromatase inhibitors together with an antiandrogen appea

270 ESR1 mutations are prevalent in ER-positive aromatase inhibitor-treated MBC.

271 In first-line aromatase inhibitor-treated patients (n=2252), the media

272 ligand antibody denosumab in postmenopausal, aromatase inhibitor-treated patients with early-stage ho

273 ived from a further independent cohort of 72 aromatase inhibitor-treated patients.

274 cer whose disease had progressed on or after aromatase inhibitor treatment and had received up to one

275 n part 2, we stratified patients by previous aromatase inhibitor treatment for advanced or metastatic

276 e or relapse during or within 6 months of an aromatase inhibitor treatment in the adjuvant setting an

277 more importantly, predicted poor response to aromatase inhibitor treatment with the development of re

278 act of GDNF-RET signaling in the response to aromatase inhibitor treatment.

279 lated with suppression of proliferation upon aromatase inhibitor treatment.

280 W embryonic gonads that were masculinized by aromatase inhibitor treatment.

281 responding rapidly to temperature shifts and aromatase inhibitor treatment.

282 a negative association with the efficacy of aromatase-inhibitor treatment.

283 rding Hologic device for DXA scans, previous aromatase inhibitor use, and baseline bone mineral densi

284 k) or relapse (after > or = 2 y) of adjuvant aromatase inhibitor use.

285 The use of aromatase inhibitors was associated with a significantly

286 AR, 24.1); however, initiating therapy with aromatase inhibitors was not associated with VTE (HR, 0.

287 compounds library of our earlier synthesized aromatase inhibitors was performed and, according to the

288 breast cancer progressing on a nonsteroidal aromatase inhibitor were randomly assigned to exemestane

289 cancer who had relapsed or progressed on an aromatase inhibitor were recruited from 19 hospitals in

290 Aromatase inhibitors were associated with a significantl

291 Aromatase inhibitors were associated with elevated HRs,

292 In this population-based study, aromatase inhibitors were associated with increased risk

293 Tamoxifen, raloxifene, and aromatase inhibitors were associated with lower risk of

294 itive breast cancer receiving treatment with aromatase inhibitors were randomly assigned in a 1:1 rat

295 matase inhibitor or tamoxifen followed by an aromatase inhibitor, were randomly assigned (1:1) to rec

296 s and of the side effects of cytochrome P450 aromatase inhibitors, which are frequently used for brea

297 had metastatic breast cancer treated with an aromatase inhibitor with progression-free survival (> or

298 os (HRs) with 95% CIs comparing new users of aromatase inhibitors with new users of tamoxifen for eac

299 As aromatase inhibitors work by inhibiting the conversion o

300 We postulated that an aromatase inhibitor would be safer and more effective.