ライフサイエンスコーパス: aromatase

1 via the intracrine activities of SRD5A1 and aromatase.

2 reases in acetyl-HIF-1alpha, HIF-1alpha, and aromatase.

3 uction of acetyl-HIF-1alpha, HIF-1alpha, and aromatase.

4 in the nucleus of the solitary tract express aromatase.

5 cellular identities of neurons that express aromatase.

6 tween the peripheral immune system and brain aromatase.

7 rough differential production via the enzyme aromatase.

8 ic activity of the estrogen-producing enzyme aromatase.

9 from androgens via the action of the enzyme aromatase.

10 of postmenopausal breast tumors overexpress aromatase.

11 phalic aromatase activity and immunoreactive aromatase (24 hour time point only).

12 mediators responsible for local induction of aromatase, a rate-limiting enzyme in estrogen biosynthes

13 via peripheral endotoxin increases neuronal aromatase; a mechanism that may rapidly generate a poten

14 CYP19A1 amplification caused increased aromatase activity and estrogen-independent ERalpha bind

15 romatase was measured, as were telencephalic aromatase activity and immunoreactive aromatase (24 hour

16 Mechanical wounding reduced fibroblast aromatase activity but increased keratinocyte activity,

17 of adipose tissue (eg, via other adipokines, aromatase activity) could also be involved in changes to

18 R (qRT-PCR) mRNA expression, enzymatic assay aromatase activity, scratch assay cell migration, immuno

19 cts can be mediated via local alterations in aromatase activity, which precisely regulates the tempor

20 uced proliferation of beta-cells depended on aromatase activity.

21 psed patients had acquired CYP19A1 (encoding aromatase) amplification (CYP19A1(amp)).

22 Genetic variation in aromatase and changes in estrogen metabolites were assoc

23 isplayed elevated inhibitory potency against aromatase and enhanced affinity for estrogen receptors w

24 (1) lacked the normal elevation of astrocyte aromatase and hippocampal E2 levels; (2) had significant

25 Increased concentrations of aromatase and interleukin 6 in inflamed breast tissue an

26 measures to examine the relationship between aromatase and personality traits related to self-regulat

27 emia, reactive astrocytes express the enzyme aromatase and produce 17beta-estradiol (E2), although th

28 time that p53 is a key negative regulator of aromatase and, hence, estrogen production in the breast

29 including those for the estrogen receptors, aromatases, and vitellogenins.

30 ERs and aromatase are expressed across the nervous system, inclu

31 hat the 5alpha-R type 1 isoform (SRD5A1) and aromatase are expressed in male and female beta-cells.

32 ere we provide evidence that cytochrome P450 aromatase (AROM), the enzyme converting testosterone to

33 A ToxCast aromatase assay provided concentration-inhibition relati

34 e measurement of baseline and post-treatment aromatase availability in primary tumors and metastatic

35 ve measurement of baseline and posttreatment aromatase availability in primary tumors and metastatic

36 We measured aromatase availability in the amygdala using positron em

37 Results indicated that aromatase availability in the amygdala was negatively as

38 and evaluated for their abilities to inhibit aromatase, bind to estrogen receptor alpha (ER-alpha) an

39 xpression levels of the rate-limiting enzyme aromatase, but not estrogen receptors, measured by qPCR

40 Human aromatase catalyzes the synthesis of estrogen from andro

41 owever, the developmental etiology of ER and aromatase cellular expression in female and male striatu

42 Thus, ERalpha, GPER1, and aromatase cellular immunoreactivity was assessed in peri

43 NAs targeting an estrogen receptor (ER)- and aromatase-centered network identified 46 genes that are

44 Aromatase clusters were also more abundant and tightly p

45 d higher levels of Hsp90 ATPase activity and aromatase compared with wild-type stromal cells.

46 indirectly via the estrogen receptor through aromatase conversion to estradiol, we further examined h

47 sulin resistance while exhibiting suppressed aromatase (Cyp19a1) expression and reduced circulating 1

48 yclin A1 expression was also correlated with aromatase (CYP19A1), a key enzyme that directly regulate

49 Aromatase (CYP19A1), the enzyme that converts androgens

50 s steroid-specific except for genes encoding aromatase (cyp19b), sulfotransferase (sult2st3), and cyp

51 e-nucleotide polymorphism (SNP) rs7175922 in aromatase (cytochrome P450 family 19 subfamily A member

52 ding IMiDs in multiple myeloma (MM), lead to aromatase degradation in human megakaryocytes.

53 In the bone marrow, cyclin A1 and aromatase enhanced local bone marrow-releasing factors,

54 ty but also for estradiol production via the aromatase enzyme and estradiol action via the alpha isof

55 by prostaglandin E2 (PGE2) activation of the aromatase enzyme, as we reported previously and confirm

56 on of the proliferation marker Ki-67 and the aromatase enzyme.

57 ctive estrogen 17beta-estradiol (E2) via the aromatase enzyme.

58 differences in the cellular distribution of aromatase (estrogen synthase) in several species suggest

59 w in rats that systemic administration of an aromatase (estrogen synthase) inhibitor after seizure on

60 sted the hypothesis that ERalpha, GPER1, and aromatase exhibits sex, region, and age-specific differe

61 We find that activity of aromatase-expressing BNSTpr (AB) neurons appears to enco

62 romogenic in situ hybridization we localized aromatase-expressing cells to ependymal regions borderin

63 unocytochemistry revealed greater numbers of aromatase-expressing neurons in LPS birds.

64 cytoarchitecture and cellular identities of aromatase-expressing neurons in the auditory and sensori

65 Ablation of the oxytocin receptor in aromatase-expressing neurons of the medial amygdala (MeA

66 Notably, aromatase-expressing neurons were found in dense somato-

67 However, conceptus aromatase expression and estrogen secretion were decreas

68 We did not find sex differences in aromatase expression and neither the pattern nor the num

69 vorozole is a useful technique for measuring aromatase expression in individual breast lesions, enabl

70 vorozole is a useful technique for measuring aromatase expression in individual breast lesions, enabl

71 activity, levels of PKM2 and HIF-1alpha, and aromatase expression in LFS stromal cells.

72 lencing either HIF-1alpha or PKM2 suppressed aromatase expression in LFS stromal cells.

73 nsity and distribution of astrocytes, normal aromatase expression in neurons, and normal cognitive fu

74 timize PET with (11)C-vorozole for measuring aromatase expression in postmenopausal breast cancer in

75 aphy (PET) with (11)C-vorozole for measuring aromatase expression in postmenopausal breast cancer.

76 Somatic aromatase expression presents at prepuberty and increase

77 Aromatase expression was observed in radial glial cells,

78 This brain aromatase expression was positively correlated with circ

79 etween HIF-1alpha and p300, a coactivator of aromatase expression, and suppressed p300 binding to the

80 First, we found that brain aromatase expression, and thus the capacity to synthesiz

81 ctivated glucocorticoid receptor, decreasing aromatase expression, induces Leydig tumor regression bo

82 Although p53 down-regulates aromatase expression, the underlying mechanisms are inco

83 Inhibition of Hsp90 ATPase suppressed aromatase expression.

84 ibition of Hsp90 ATPase activity and reduced aromatase expression.

85 hether SIRT1 also plays a role in regulating aromatase expression.

86 IF-1alpha and HIF-1alpha levels and enhanced aromatase gene transcription.

87 ated glucocorticoid receptor to regulate the aromatase gene transcriptional activity through the recr

88 For the past 40 years, aromatase has been a target of intense inhibitor discove

89 are synthesized from androgens by the enzyme aromatase, highly expressed in the ovaries of reproducti

90 e and female zebra finches, a combination of aromatase immunohistochemistry and conventional tract tr

91 (HIF-1alpha) contribute to the induction of aromatase in adipose stromal cells (ASCs).

92 ontrast, calbindin was not co-expressed with aromatase in any region investigated.

93 levels of acetyl-HIF-1alpha, HIF-1alpha, and aromatase in breast tissue of obese compared with lean w

94 1alpha contributes to the elevated levels of aromatase in breast tissues of obese women.

95 erneuron subtypes, and are co-expressed with aromatase in human temporal cortex.

96 M2/HIF-1alpha axis mediates the induction of aromatase in LFS.

97 decreased Th1 and Th17 differentiation in an aromatase-independent fashion, but also exacerbated cell

98 ibitor anastrazole and were increased by the aromatase inducer dexamethasone.

99 campal estrogen synthesis, intra-hippocampal aromatase inhibition also suppressed seizures.

100 uption via exogenous chemicals requires that aromatase inhibition be considered in addition to androg

101 urons in rodent BLA responded differently to aromatase inhibition both in vivo and in vitro, our find

102 arning models utilizing different sources of aromatase inhibition data are described.

103 itutitary-gonadal axis in female FHMs, where aromatase inhibition decreases the conversion of testost

104 These methods to predict aromatase inhibition from molecular structure, when used

105 cability for a previously described qAOP for aromatase inhibition leading to decreased fecundity deve

106 The resulting total aromatase inhibition was input to a mathematical model o

107 Further, chronic aromatase inhibition within the dentate gyrus blocked th

108 onvenient to functionalize to reach superior aromatase inhibition.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 RATIONALE: The aromatase inhibitor anastrozole blocks the conversion of

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

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

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

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

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

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

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

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

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

143 e cyclooxygenase inhibitor nimesulide or the aromatase inhibitor formestane.

144 14.9 months (14.0-16.7) in the placebo plus aromatase inhibitor group (difference 13.1 months; range

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 responding rapidly to temperature shifts and aromatase inhibitor treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 be administered with either tamoxifen or an aromatase inhibitor.

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

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

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

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

188 Aromatase inhibitors (AI) are associated with significan

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

190 Aromatase inhibitors (AI) induce painful musculoskeletal

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

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

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

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

195 Aromatase inhibitors (AIs) are the standard endocrine th

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

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

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

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

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

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

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

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

204 Aromatase inhibitors (AIs) prevent estrogen production a

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

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

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

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

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

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

211 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

212 The association between aromatase inhibitors and cardiovascular outcomes among w

213 Aromatase inhibitors are a standard of care for hormone

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

215 Purpose Aromatase inhibitors are established breast cancer chemo

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

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

218 Aromatase inhibitors are the mainstay of hormonal therap

219 Introduction: Aromatase inhibitors are the mainstay of hormonal therap

220 Aromatase inhibitors are the preferred treatment for cer

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

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

223 0.24-0.80]; 2 trials [n = 17 806]), and the aromatase inhibitors exemestane and anastrozole (RR, 0.4

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

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

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

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

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

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

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

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

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

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

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

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

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

237 The use of aromatase inhibitors was associated with a significantly

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

239 Aromatase inhibitors were associated with a significantl

240 Aromatase inhibitors were associated with elevated HRs,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 mutations associate with a lower response to aromatase inhibitors.

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

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

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

259 The potent aromatase inhibitory activities and high ER-alpha and ER

260 Compounds with both aromatase inhibitory and estrogen receptor modulatory ac

261 f the 17beta-estradiol (E2) synthesis enzyme aromatase is highly upregulated in astrocytes following

262 Aromatase is the enzyme responsible for synthesis of E2

263 illary acidic protein (GFAP) promoter-driven aromatase knock-out (GFAP-ARO-KO) mouse model to deplete

264 illary acidic protein (GFAP) promoter-driven aromatase knock-out (GFAP-ARO-KO) mouse to deplete astro

265 Here, we used a forebrain neuron-specific aromatase KO (FBN-ARO-KO) mouse model to deplete neuron-

266 emales that are close to spawning had higher aromatase levels in all brain regions compared to female

267 and cytokines had returned to baseline, but aromatase mRNA and activity were elevated in both sexes.

268 from women with obesity displayed increased aromatase mRNA compared with lean controls.

269 neurons, and ventromedial to this, an ovoid, aromatase-negative (AR-) nucleus.

270 In total, given their location, these aromatase neurons are poised to engage nociceptive circu

271 from human cortex by identifying a subset of aromatase neurons as putative inhibitory interneurons.

272 A few aromatase neurons express Fos after cheek injection of c

273 Aromatase, or cytochrome P450 19A1, catalyzes the aromat

274 man SynT differentiation, including hCYP19A1/aromatase P450, glial cells missing 1 (GCM1), frizzled 5

275 regulates the expression of cytochrome P450 aromatase (P450arom).

276 n the basal hypothalamus: an oblique band of aromatase-positive (AR+) neurons, and ventromedial to th

277 of HIF-1alpha and PKM2 was recruited to the aromatase promoter II in LFS stromal cells.

278 glucocorticoid responsive element within the aromatase promoter II.

279 pression, and suppressed p300 binding to the aromatase promoter.

280 the publication of the crystal structure of aromatase purified from human placenta, revealing an and

281 Immunohistochemical staining in an aromatase reporter mouse revealed that many neurons in l

282 steroidogenic enzyme [cytochrome P450(CYP19) aromatase] required for estrogen synthesis in vertebrate

283 To optimize its efficacy and aromatase selectivity versus other cytochrome P450 enzym

284 h) tumor cells expressing elevated levels of aromatase stimulated tumor/host estrogen production and

285 Here we report that the aromatase substrate androstenedione, unique among severa

286 oups, with mean SUV in tumors overexpressing aromatase (SUVR>1.1) ranging from 2.47 to 13.6, while tu

287 .47 to 13.6, while tumors not overexpressing aromatase (SUVR<1) ranged from 0.8 to 1.8.

288 ge between inhibition of cytochrome P450 19A aromatase (the MIE) and population-level decreases in th

289 estrogen, here we examined the expression of aromatase, the enzyme that catalyzes the conversion of t

290 Aromatase, the last and obligatory enzyme catalyzing est

291 Recently, elevated levels of aromatase, the rate-limiting enzyme for estrogen biosynt

292 Levels of aromatase, the rate-limiting enzyme in estrogen biosynth

293 ns are derived from androgens via the enzyme aromatase), they subserve markedly different functions v

294 cimens from the same tumors were stained for aromatase using immunohistochemistry and evaluated for s

295 Aromatase was co-expressed with parvalbumin in the caudo

296 The central transcription of cytokines and aromatase was measured, as were telencephalic aromatase

297 ockout mouse models for estrogen receptor or aromatase, we observed that perturbation in estrogen tra

298 and antagonists following blockade of brain aromatase, we show here that brain-derived estrogens acu

299 ATPase activity, Aha1, HIF-1alpha, PKM2, and aromatase were increased in the mammary glands of p53 nu

300 tic plasticity in the BLA involving neuronal aromatase, which produces the neurosteroid 17beta-estrad