ライフサイエンスコーパス: aromatase inhibitor

1 effect of dihydrotestosterone and letrozole (aromatase inhibitor).

2 hereby abrogating synthesis of this hormone (aromatase inhibitors).

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

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

5 rs clinically responsive and resistant to an aromatase inhibitor.

6 rticularly those considering therapy with an aromatase inhibitor.

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

8 be administered with either tamoxifen or an aromatase inhibitor.

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

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

11 ed by adjuvant therapy with antiestrogens or aromatase inhibitors.

12 signed and synthesized as nonsteroidal CYP19 aromatase inhibitors.

13 he development of new pyrroloquinoline-based aromatase inhibitors.

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

15 cancer previously treated with nonsteroidal aromatase inhibitors.

16 pallium) cytoarchitecture in the presence of aromatase inhibitors.

17 dict interpatient variability in response to aromatase inhibitors.

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

19 l lacking in pediatric patients treated with aromatase inhibitors.

20 uated prospectively in patients treated with aromatase inhibitors.

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

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

23 d arthritis) are a well-known side-effect of aromatase inhibitors.

24 tudies have focused on adherence to adjuvant aromatase inhibitors.

25 sinone II derivatives that were evaluated as aromatase inhibitors.

26 good candidates for targeted treatment with aromatase inhibitors.

27 ps after an initial response to tamoxifen or aromatase inhibitors.

28 enedione into estrogens and was sensitive to aromatase inhibitors.

29 trant is also an option after treatment with aromatase inhibitors.

30 no longer sensitive to growth inhibition by aromatase inhibitors.

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

32 cancer patients, predominantly treated with aromatase inhibitors.

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

34 ET, evenly distributed between tamoxifen or aromatase inhibitors.

35 roid sulfatase inhibitory pharmacophore into aromatase inhibitor 1 (YM511), two series of single agen

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

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

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

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

40 nomical synthesis of the naturally occurring aromatase inhibitor abyssinone II was performed.

41 e in postmenopausal women, but non-steroidal aromatase inhibitors accelerate bone loss and increase f

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

43 ubing containing testosterone (T), T plus an aromatase inhibitor (ADT), or 5alpha-dihydrotestosterone

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

45 formation exists on the long-term effects of aromatase inhibitors after treatment, and whether these

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

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

48 e time to progression (TTP) with a steroidal aromatase inhibitor (AI) atamestane (ATA) combined with

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

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

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

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

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

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

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

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

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

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

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

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

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

62 In these experiments the aromatase inhibitor (AI), 4-hydroxy androstenedione (4-O

63 study initiation, 13% of patients were on an aromatase inhibitor (AI).

64 th disease progression on a third-generation aromatase inhibitor (AI).

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

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

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

68 Aromatase inhibitors (AI) are associated with significan

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

70 Aromatase inhibitors (AI) are rapidly becoming the first

71 Acquired resistance to either tamoxifen or aromatase inhibitors (AI) develops after prolonged treat

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

73 Aromatase inhibitors (AI) induce painful musculoskeletal

74 Food and Drug Administration (FDA)-approved aromatase inhibitors (AI) on aromatase protein stability

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

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

77 50% of breast cancer survivors treated with aromatase inhibitors (AIs) and is the most common reason

78 Aromatase inhibitors (AIs) are effective for treatment o

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

80 Aromatase inhibitors (AIs) are now established as adjuva

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

82 Aromatase inhibitors (AIs) are the standard endocrine th

83 en receptor-positive breast cancer receiving aromatase inhibitors (AIs) as part of their adjuvant the

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

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

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

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

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

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

90 Aromatase inhibitors (AIs) improve survival in postmenop

91 omized trials have evaluated the role of the aromatase inhibitors (AIs) in postmenopausal women with

92 Aromatase inhibitors (AIs) increase the risk of osteopor

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

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

95 Aromatase inhibitors (AIs) prevent estrogen production a

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

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

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

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

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

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

102 logical testosterone in conjunction with the aromatase inhibitor anastrazole (Tfm, n=7).

103 nib (250 mg given orally once a day) and the aromatase inhibitor anastrozole (1 mg given orally once

104 RATIONALE: The aromatase inhibitor anastrozole blocks the conversion of

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

106 Although the aromatase inhibitor anastrozole has been shown to be ver

107 The aromatase inhibitor anastrozole inhibits estrogen synthe

108 The aromatase inhibitor anastrozole was compared with tamoxi

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

110 cer and subsequently treated with one of the aromatase inhibitors (anastrozole, letrozole, exemestane

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

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

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

114 eatment with exemestane after a nonsteroidal aromatase inhibitor and vice versa.

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

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

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

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

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

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

121 Aromatase inhibitors are a standard of care for hormone

122 comprehensive studies were warranted because aromatase inhibitors are being used increasingly in both

123 Purpose Aromatase inhibitors are established breast cancer chemo

124 Aromatase inhibitors are important drugs to treat estrog

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

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

127 Aromatase inhibitors are proving to be more effective th

128 Aromatase inhibitors are the major first-line treatment

129 trogens and blocking estrogen synthesis with aromatase inhibitors are two strategies currently being

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

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

132 Aromatase inhibitors are widely used in breast cancer an

133 ial effect on the choice of tamoxifen versus aromatase inhibitors as adjuvant endocrine therapy.

134 with tamoxifen followed by cross over to an aromatase inhibitor at 2.5 years yielded a modest improv

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

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

137 Aromatase inhibitors avoid the need for external beam ra

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

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

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

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

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

143 Use of bisphosphonates in women taking aromatase inhibitors (combined with ovarian suppression

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

145 Treatment with aromatase inhibitors decreases bone mineral density (BMD

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

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

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

149 Aromatase inhibitors effectively prevent breast cancer r

150 ind clinical trial to evaluate the steroidal aromatase inhibitor exemestane as extended adjuvant ther

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

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

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

154 al that compared the switch to the steroidal aromatase inhibitor exemestane with continuation of tamo

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

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

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

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

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

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

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

162 ficial strategy to prolong responsiveness to aromatase inhibitors for patients with breast cancer.

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

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

165 e cyclooxygenase inhibitor nimesulide or the aromatase inhibitor formestane.

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

167 pubertal gynecomastia, but treatment with an aromatase inhibitor has not been shown to be more effect

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

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

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

171 Aromatase inhibitors have been reported to increase heig

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

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

174 mers, ( R)-phenol ( 39a) was the most potent aromatase inhibitor (IC 50 = 0.6 nM, comparable to letro

175 Although aromatase inhibitors improve disease-free survival, tamo

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

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

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

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

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

181 or reverse the development of resistance to aromatase inhibitors in advanced breast cancer patients.

182 Third-generation aromatase inhibitors in combination with antiandrogens a

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

184 MCF-7aro cells, the physiologically relevant aromatase inhibitors in mushrooms are most likely conjug

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

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

187 The widening use of aromatase inhibitors in the adjuvant setting, however, m

188 an stimulation can be minimized by utilizing aromatase inhibitors in women with estrogen-sensitive ca

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

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

191 gh an effective treatment for breast cancer, aromatase inhibitors indiscriminately abolish estrogen s

192 ear factor-kappaB ligand, to protect against aromatase inhibitor-induced bone loss.

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

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

195 isease-free survival have been noted when an aromatase inhibitor is given either instead of or sequen

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

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

198 he new generation of hormone therapies named aromatase inhibitors, is reported.

199 Aromatase inhibitors lead to profound estrogen suppressi

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

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

202 rogen-deprivation therapy in the form of the aromatase inhibitor letrozole has demonstrated activity

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

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

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

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

207 and anastrozole) and steroidal (exemestane) aromatase inhibitors may allow treatment with exemestane

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

209 l carcinomas, and opens the possibility that aromatase inhibitors may be potential therapeutic agents

210 In conclusion, the results suggest that aromatase inhibitors may exert their antiproliferative e

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

212 Aromatase inhibitors might be more efficacious, and resu

213 ared with 82.6% and 65.5%, respectively, for aromatase inhibitor monotherapy, which is a 6% relative

214 disease-free survival compared with planned aromatase inhibitor monotherapy.

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

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

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

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

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

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

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

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

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

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

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

226 Aromatase inhibitors play a prominent role in the manage

227 Aromatase inhibitors prevent breast cancer in postmenopa

228 Aromatase inhibitors prevent more contralateral breast c

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

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

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

232 Aromatase inhibitors represent a new generation of hormo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

248 ons of the gastroprotective and nonsteroidal aromatase inhibitor sesquiterpene lactone ludartin, isol

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

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

251 Aromatase inhibitors target the production of estrogen i

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

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

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

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

256 bitor therapy were stratified by duration of aromatase inhibitor therapy (< or = 6 v > 6 months), rec

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

258 Adjuvant aromatase inhibitor therapy is well established in postm

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

260 ree of the beneficial carryover effect after aromatase inhibitor therapy or the ratio of local to dis

261 tastatic breast cancer treated with adjuvant aromatase inhibitor therapy were stratified by duration

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

263 month and were not influenced by duration of aromatase inhibitor therapy.

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

265 Aromatase inhibitors therefore constitute a frontline th

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

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

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

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

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

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

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

273 The application of aromatase inhibitors to postmenopausal breast cancer pat

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

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

276 Aromatase inhibitors together with an antiandrogen appea

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

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

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

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

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

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

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

284 responding rapidly to temperature shifts and aromatase inhibitor treatment.

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

286 lated with suppression of proliferation upon aromatase inhibitor treatment.

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

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

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

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

291 The most potent of the achiral and racemic aromatase inhibitor was 40 (IC 50 = 3.0 nM).

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

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

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

295 Aromatase inhibitors were associated with a significantl

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

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

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

299 As aromatase inhibitors work by inhibiting the conversion o

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