ライフサイエンスコーパス: androgen

1 is often aberrantly activated independent of androgen.

2 ) allele increases DHEA metabolism to potent androgens.

3 ead to changes in enterohepatic recycling of androgens.

4 lamin-dependent estrogen methylation to form androgens.

5 cyprodinil, and dimethomorph as in vivo anti-androgens.

6 mparison between the prenatal oestrogens and androgens.

7 y are established in early life by perinatal androgens.

8 s of E2 rather than an increase in precursor androgens.

9 Amongst these were an androgen, 5alpha-androstane 3,17-dione, detected as the

10 Androgen ablation combined with PARG inhibition synergis

11 A combination of PARG inhibition with androgen ablation or with the DNA damaging drug, temozol

12 al regulation suggesting that the success of androgen ablation therapy can be enhanced by PARG inhibi

13 genetic evidence that Sox2 is necessary for androgen ablation-induced neuroendocrine differentiation

14 cquire enhanced regenerative potential after androgen ablation.

15 productive toxicity related to disruption of androgen action during fetal life is difficult to predic

16 s bind to human SHBG, and how they influence androgen activity in cell culture.

17 eatments such as chemotherapy and novel anti-androgen agents has further hampered progress.

18 These adrenal-derived androgens all share an oxygen atom on carbon 11, so we h

19 in DHT3 capable of catabolizing estrogens or androgens anaerobically.

20 tase inhibition be considered in addition to androgen and estrogen pathway interference.

21 vanced prostate cancer, and an enrichment of androgen and Wnt signaling activation has been observed

22 d with the naturally high level of perinatal androgens and can be recapitulated in females by perinat

23 e equilibrium between free and protein-bound androgens and estrogens in the blood and regulates their

24 enal dehydroepiandrosterone (DHEA) to potent androgens and has a germline missense-encoding polymorph

25 f autistic boys, based on measuring prenatal androgens and other steroid hormones.

26 INPP4B is up-regulated by androgens, and this suggests that androgen-deprivation t

27 srupt the microtubule assembly and act as an androgen antagonist, and varying the second axial positi

28 state diseases, which are linked to elevated androgen, are significant risk factors and that genetic

29 Confirmation of these androgens as alternate biomarkers of near-term pregnancy

30 e variants in DENND1A, a gene that regulates androgen biosynthesis, were significantly more likely to

31 A-disrupted DHT3 derivative could catabolize androgens but not estrogens.

32 Following puberty, the synthesis of androgens by the adrenal gland has been considered of li

33 Estrogens are synthesized from androgens by the enzyme aromatase, highly expressed in t

34 rity of motor symptoms, whereas elevation of androgens can exacerbate tic disorders.

35 to the more extensively studied, traditional androgens, circulating concentrations of 11-oxyandrogens

36 HDL, insulin resistance as well as increased androgens compared to their respective controls without

37 Thus, factors affecting levels of perinatal androgens could have a significant impact on MC developm

38 beta-catenin signaling (PKP2, UBE2R2, TNKS), androgens (CYP4A11, CYP4A22, CYP4B1, CYP4X1, CYP4Z2P, EP

39 g that initiation of meiotic prophase is not androgen dependent.

40 after the clinical transition from treatable androgen-dependent disease to untreatable CRPC.

41 ds to a putative CHPT1 enhancer and mediates androgen-dependent expression of CHPT1 gene in Enz-sensi

42 Androgen-dependent nuclear accumulation of the polygluta

43 e demonstrate that upregulation of MUC1-C in androgen-dependent PC cells suppresses androgen receptor

44 DBP exposure of recipient mice reduced androgen-dependent seminal vesicle weight (8.3 vs 26.7 m

45 ound that androgen-induced gene 1 (AIG1) and androgen-dependent TFPI-regulating protein (ADTRP), two

46 and polycystic ovary syndrome, as well as in androgen-dependent tumours, such as castration-resistant

47 ment, fertility, and lifelong health are all androgen-dependent.

48 is a hallmark of prostate cancer (PCa) with androgen deprivation being standard therapy.

49 olide) are the standard agents for achieving androgen deprivation for prostate cancer despite the ini

50 androgens suppress CDCP1 expression and that androgen deprivation in combination with loss of PTEN pr

51 Androgen deprivation is the cornerstone of prostate canc

52 berrantly high expression of m1 and m3 under androgen deprivation mimicking castration and androgen r

53 ostate cancers, including those resistant to androgen deprivation or antiandrogen therapies.

54 assigned to RP alone or neoadjuvant CHT with androgen deprivation plus docetaxel (75 mg/m(2) body sur

55 isk disease were all prescribed 24 months of androgen deprivation therapy (ADT) and had lymph node ir

56 ity regarding the influence of sequencing of androgen deprivation therapy (ADT) and radiotherapy (RT)

57 ged with the combination of radiotherapy and androgen deprivation therapy (ADT) compared with ADT alo

58 Androgen deprivation therapy (ADT) has become a standard

59 Radiotherapy in combination with androgen deprivation therapy (ADT) is a standard treatme

60 Androgen deprivation therapy (ADT) is still a mainstay o

61 Androgen deprivation therapy (ADT) is the standard care

62 GG) from transrectal US-guided biopsy, prior androgen deprivation therapy (ADT), and any prior CT res

63 d phenotypic change of prostate cancer after androgen deprivation therapy (ADT), and it ultimately de

64 Intermittent androgen deprivation therapy (IADT) is an attractive tre

65 nt with prostatectomy (n = 402) or EBRT with androgen deprivation therapy (n = 217) for men with unfa

66 l, primary Gleason score, and prior therapy (androgen deprivation therapy and external-beam radiation

67 advanced metastatic disease (n = 103), after androgen deprivation therapy only (n = 16), after surger

68 astatic tumors that have become resistant to androgen deprivation therapy represent the major challen

69 e radiotherapy and lower rates of additional androgen deprivation therapy than those with extrafossa

70 Patients on androgen deprivation therapy were excluded.

71 diation therapy (79.1% vs. 82.1%, P = 0.55), androgen deprivation therapy within the 6 mo preceding i

72 served in prostate cancer patients receiving androgen deprivation therapy, highlighting the evolution

73 Resistance to androgen deprivation therapy, or castration-resistant pr

74 from a clinical trial of neoadjuvant intense androgen deprivation therapy.

75 with prostate cancer undergoing intermittent androgen deprivation therapy.

76 we show that RUNX1(+) PLCs are unaffected by androgen deprivation, and do not contribute to the regen

77 ancer patients will initially respond to the androgen deprivation, the disease often progresses to ca

78 cal information; sRT; timing and duration of androgen deprivation; 3-y PSA results; and clinical even

79 en by androgen receptor (AR) is treated with androgen deprivation; however, therapy failure results i

80 (56.5% v 71.3%), were less likely to receive androgen-deprivation therapy (79.5% v 87.8%), and slight

81 Dose-escalated radiotherapy (RT) with androgen-deprivation therapy (ADT) is a standard definit

82 neuroendocrine prostate cancer (NEPC) after androgen-deprivation therapy (ADT) is well-known.

83 h localized prostate cancer, the addition of androgen-deprivation therapy (ADT) or a brachytherapy bo

84 gulated by androgens, and this suggests that androgen-deprivation therapy (ADT) would lead to hyperac

85 er median overall survival than placebo plus androgen-deprivation therapy among men with nonmetastati

86 l radiation therapy in 19.3% of patients and androgen-deprivation therapy in 7.4%.

87 esized that chemohormonal therapy (CHT) with androgen-deprivation therapy plus docetaxel before RP wo

88 Enzalutamide plus androgen-deprivation therapy resulted in longer median o

89 <=10 months) who were continuing to receive androgen-deprivation therapy were randomly assigned (in

90 e-specific antigen (PSA) levels while taking androgen-deprivation therapy.

91 herapy regimens in combination with standard androgen-deprivation therapy.

92 54 patients) while they continued to receive androgen-deprivation therapy.

93 ded gene knockout experiments indicated that androgen differentially regulates YAP1-dependent gene ex

94 e conversion in target tissues to the potent androgen dihydrotestosterone (DHT) via the enzyme 5alpha

95 rther examined how a potent non-aromatizable androgen, dihydrotestosterone (DHT), acts via the AR to

96 muscle invasive BCa, we first found that the androgens, dihydrotestosterone (DHT) might function via

97 lly to prostate regeneration, partly through androgen-driven expression of growth factors (Nrg2, Rspo

98 ed that penis development is not an entirely androgen-driven process but one in which endogenous estr

99 Rodent studies show that perturbation of androgens (e.g. following phthalate exposure) during a f

100 Assessment of response to the anti-androgen enzalutamide shows a distinct separation of res

101 P derivative cell line resistant to the anti-androgen, enzalutamide (LNCaP-EnzR).

102 hese findings reveal that, in the absence of androgens, ERbeta1 induces INPP4B to dampen AKT signalin

103 as major components of several disorders of androgen excess, such as congenital adrenal hyperplasia,

104 We also found that androgen exposure antagonizes Ser/Thr kinase 4 (STK4/MST

105 re to testosterone proprionate, 3) perinatal androgen exposure guides bone marrow MC progenitors towa

106 We demonstrate that androgen exposure suppresses the inactivating post-trans

107 s that express androgen receptor and require androgens for growth.

108 elucidate the mechanism of hepatic uptake of androgen glucuronides and estimate the fractional contri

109 We previously established that androgen glucuronides are effluxed by multidrug resistan

110 ucidates the mechanisms of hepatic uptake of androgen glucuronides.

111 Over the past decade, these androgens have emerged as major components of several di

112 Androgens have male-specific prenatal influence over soc

113 However, androgens have potential benefits in asthma.

114 anges were coincident with reduced levels of androgens in males and estrogens in females.

115 s a consequence, the depletion of testicular androgens in patients with prostate cancer results in tu

116 ul model species for elucidating the role of androgens in social status given their rich social hiera

117 Consistently, the estrogen conversion into androgens in strain DHT3 cell extracts requires methylco

118 is correlated with increased metastasis and androgen independence.

119 g promotes prostate cancer expansion towards androgen independent signaling, supporting a neomorphism

120 ngly, despite the decreased proliferation of androgen-independent cell no alterations in the cell cyc

121 in proliferation was remarkably specific to androgen-independent cells.

122 cer within the CHPT1 SE locus and facilities androgen-independent expression of CHPT1 in Enz-resistan

123 eening for antiproliferative activity in the androgen-independent PC3 prostate cancer cell line.

124 U87 DeltaEGFR glioblastoma, and human DU145 androgen-independent prostate carcinoma tumor cells indi

125 OS women showed increased testosterone, free androgen index, HDL and CRP (P < 0.01).

126 ion through meiosis, but the extent to which androgens indirectly regulate specific meiotic stages is

127 e role of novel exonuclease 5 (EXO5) gene in androgen-induced double strand breaks repair via homolog

128 ivity-based protein profiling, we found that androgen-induced gene 1 (AIG1) and androgen-dependent TF

129 rected recombination repair (HDR) and caused androgen-induced genomic instability, as indicated by fr

130 effect on protein stability than in partial androgen insensitive syndrome (PAIS).

131 905 androgen insensitivity syndrome (AIS)-associated loss-of

132 Moreover, AR mutants in complete androgen insensitivity syndrome (CAIS) tend to have a gr

133 Conversion of C(19) androgens into C(18) estrogens is thought to be an irrev

134 The prostate regenerates when androgen is restored, a process postulated to involve st

135 tors and that genetic variants that increase androgen levels are associated with higher disease sever

136 ed a relationship between ACC activation and androgen levels before treatment but no difference in AC

137 Androgens like testosterone have been strongly linked to

138 t length ratio (2D:4D), a proxy for prenatal androgen load, and transgender identity have been incons

139 ture, when used in concert with estrogen and androgen machine learning models, allow for a more holis

140 While androgens may function via nuclear androgen receptor (nA

141 Together, these results suggest that androgens may not only function via the classic nAR to i

142 Androgens may play a role in this male-bias by sex-diffe

143 basal-to-luminal differentiation; attenuates androgen-mediated organoid organization; and retards pos

144 gests that retroconversion of estrogens into androgens occurs in the biosphere.

145 d 2D:4D indicating the influence of prenatal androgen on the development of gender identity in subjec

146 dder cancer (BCa) progression, the impact of androgens on muscle invasive BCa, which contains nearly

147 eased steroid hormones, including estrogens, androgens or glucocorticoids during pregnancy results in

148 To dissect the androgens potential impacts on these nAR-negative muscle

149 nd its sulfate, DHEAS, are the major adrenal androgen precursors, but they are biologically inactive.

150 The second most abundant unconjugated androgen produced by the human adrenals is 11beta-hydrox

151 These data, along with the observed androgen production in estrogen-fed strain DHT3 cultures

152 Glucocorticoids inhibit adrenal androgen production.

153 (sult2st3), and cyp2k22 that were induced by androgens, progestins, and glucocorticoids.

154 Androgen receptor (AR) action is a hallmark of prostate

155 ought to reconcile the clear contribution of androgen receptor (AR) activity that has been establishe

156 BRD9 interacts with androgen receptor (AR) and CCCTC-binding factor (CTCF),

157 The androgen receptor (ar) and cytochrome P450 1A genes were

158 link ligand chemical structures to MIEs for androgen receptor (AR) and glucocorticoid receptor (GR)

159 ed LNCaP proliferation, along with decreased androgen receptor (AR) and increased Nkx3.1 cellular exp

160 tochondrial deacetylase sirtuin 3 (SIRT3) by androgen receptor (AR) and its coregulator steroid recep

161 r develops very slowly in most men, with the androgen receptor (AR) and MYC transcription factors amo

162 The androgen receptor (AR) antagonist enzalutamide is one of

163 -C in androgen-dependent PC cells suppresses androgen receptor (AR) axis signaling and induces the ne

164 ssion, which is largely driven by functional Androgen Receptor (AR) expression.

165 chaperones such as Hsp40 and Hsp70 hold the androgen receptor (AR) in an inactive conformation.

166 We focused on the function of the androgen receptor (AR) in HCC and tried to find new trea

167 The androgen receptor (AR) is a critical therapeutic target

168 The androgen receptor (AR) is a target of interest for endoc

169 The androgen receptor (AR) is a type I nuclear hormone recep

170 such as ERalpha, the activation function of androgen receptor (AR) is largely dependent on its ligan

171 Inhibition of the androgen receptor (AR) is the main strategy to treat adv

172 The androgen receptor (AR) is the major driver of prostate c

173 Prostate cancer (CaP) driven by androgen receptor (AR) is treated with androgen deprivat

174 that the chromatin structure surrounding the androgen receptor (AR) locus is altered in the prostate

175 Although more than 1,000 androgen receptor (AR) mutations have been identified an

176 Since testosterone can work directly via the androgen receptor (AR) or indirectly via the estrogen re

177 Many pesticides can antagonize the androgen receptor (AR) or inhibit androgen synthesis in

178 e-genome duplication, A. burtoni possess two androgen receptor (AR) paralogs, ARalpha and ARbeta, pro

179 cancer (PCa) cells heavily rely on an active androgen receptor (AR) pathway for their survival.

180 Recent studies indicated that the androgen receptor (AR) plays important roles in modulati

181 We were also able to identify the androgen receptor (AR) point mutation T878A from 7.5 mL

182 While androgen receptor (AR) primarily binds to a putative CHP

183 Androgen receptor (AR) protein levels were increased in

184 and P63 and loss in DACH1 and PURalpha, two androgen receptor (AR) repressors.

185 (polyQ) tract polymorphism within the human androgen receptor (AR) shows population heterogeneity.

186 Loss of androgen receptor (AR) signaling dependence occurs in ap

187 Androgen receptor (AR) signaling in Sertoli cells is kno

188 Androgen receptor (AR) signaling is central to PCa and P

189 cancerous phenotype and maintains downstream androgen receptor (AR) signaling pathways.

190 ced prostate cancer therapies aim to inhibit androgen receptor (AR) signaling.

191 Androgen receptor (AR) signalling is essential in nearly

192 Enz resistance that may involve inducing the androgen receptor (AR) splicing variant 7 (ARv7).

193 DECR1 is a negatively-regulated androgen receptor (AR) target gene and, therefore, may p

194 We show that PARG is a direct androgen receptor (AR) target gene.

195 Resistance to androgen receptor (AR) targeting therapeutics in prostat

196 The androgen receptor (AR) transcription factor is a master

197 2 (CHK2) is a critical negative regulator of androgen receptor (AR) transcriptional activity, prostat

198 (PCa) genomic data, and found that BMI1 and androgen receptor (AR) were positively correlated, sugge

199 denced by the dependency of PCa cells on the androgen receptor (AR), a prostate master transcription

200 teins elevated in mutant ER cells, including androgen receptor (AR), chitinase-3-like protein 1 (CHI3

201 Androgen receptor (AR), is a transcription factor and a

202 ent tumors typically remain dependent on the androgen receptor (AR), non-AR-driven tumors that also e

203 sor by targeting several proteins, including androgen receptor (AR), steroid receptor coactivator 3 (

204 xpress estrogen receptor alpha (ERalpha) and androgen receptor (AR), suggesting changing levels of go

205 Emergence of an aggressive androgen receptor (AR)-independent neuroendocrine prosta

206 nce with the widespread use of highly potent androgen receptor (AR)-pathway inhibitors (APIs) such as

207 DOT1L selectively impaired the viability of androgen receptor (AR)-positive PCa cells and organoids,

208 tibody that internalizes in cells expressing androgen receptor (AR)-regulated prostate-specific enzym

209 Despite the clinical success of Androgen Receptor (AR)-targeted therapies, reactivation

210 ostate cancer that expressed the full-length androgen receptor (AR).

211 ucleotide expansion in the gene encoding the androgen receptor (AR).

212 While androgens may function via nuclear androgen receptor (nAR) to increase bladder cancer (BCa)

213 imately promote DNA double-strand breaks and androgen receptor activation in prostate epithelial cell

214 Androgen receptor activation is an important factor in t

215 cribe the Collaborative Modeling Project for Androgen Receptor Activity (CoMPARA) efforts, which foll

216 Ivermectin potentiated activity of anti-androgen receptor and anti-EGFR drugs in prostate and EG

217 matin for steroid hormone receptors, such as androgen receptor and estrogen receptor(1-4), but mechan

218 of predominantly luminal cells that express androgen receptor and require androgens for growth.

219 Herein, we investigated the role of androgen receptor and TES on the inflammatory response a

220 A weak androgen receptor antagonism was identified, whereas no

221 were divided in five groups (n = 10/group): androgen receptor antagonist (flutamide); estrogen recep

222 mide (MDV3100) is a potent second-generation androgen receptor antagonist approved for the treatment

223 Advanced prostate cancers resistant to androgen receptor antagonists are still susceptible to n

224 positive outcomes for non-metastatic PC with androgen receptor antagonists, respectively.

225 ng a 6-fold difference in log-probability of androgen receptor binding at the variant rs2680708 (17q2

226 ion signature, which revealed enrichment for androgen receptor binding sequences and hypomethylation

227 that genes in this factor were enriched for androgen receptor binding sites.

228 Surprisingly, androgen receptor controls a splicing program distinct f

229 aryl pyrazol-1-yl-propanamides as selective androgen receptor degraders (SARDs) and pan-antagonists

230 rowth and motility, a known signal to bypass androgen receptor dependence.

231 However, inhibition of androgen receptor did not lead to increased phosphorylat

232 With no or a very low level of androgen receptor expression, the tumor cells were resis

233 prescribed for CRPC which works by blocking androgen receptor function.

234 Deletion of androgen receptor in GHRH neurons only delayed female pu

235 A9) was recently characterized as a membrane androgen receptor in various teleost and mammalian cell

236 ndrogen deprivation mimicking castration and androgen receptor inhibition.

237 xpression, the tumor cells were resistant to androgen receptor inhibition.

238 nhanced neuritogenesis in the presence of an androgen receptor inhibitor to the extent seen in ED pep

239 e-cell RNAseq (scRNAseq) in the Sertoli-cell androgen receptor knockout (SCARKO) mutant and control m

240 was found to be independent of the canonical androgen receptor pathway.

241 There is mounting evidence of androgen receptor signaling inducing genome instability

242 ply a marker of resistance to 2nd-generation androgen receptor signaling inhibitors (ARSi) like abira

243 rall survival times in patients treated with androgen receptor signaling inhibitors and taxanes.

244 and genetic experiments revealed that intact androgen receptor signaling is necessary for androgen's

245 nd candidate resistance mechanisms including androgen receptor signaling, mucin overexpression and an

246 The blockage of androgen receptor significantly increased radiographic b

247 Expression of the androgen receptor splice variant 7 (AR-V7) is frequently

248 The role of truncated androgen receptor splice variant-7 (AR-V7) in prostate c

249 Treatment-refractory, constitutively active androgen receptor splice variants promote hepatocellular

250 ls to be AE1/AE3, CK7, GCDFP-15, E-cadherin, androgen receptor stain and GATA3 positive.

251 sitivity and the second documented case with androgen receptor stain positivity.

252 e Cancer Genome Atlas revealed that YAP1 and androgen receptor transcript levels correlate with each

253 NA damage/replication stress response, TP53, androgen receptor, phosphatidylinositol-3-kinase/AKT, an

254 lling of key regulatory cascades such as the androgen receptor, PI3K-AKT or GATA2-dependent pathways,

255 in prostate adenocarcinoma are driven by the androgen receptor, providing opportunities for functiona

256 n disease onset and progression through both androgen receptor-dependent and androgen receptor-indepe

257 ed after one to two lines of next-generation androgen receptor-directed therapy and one taxane-based

258 through both androgen receptor-dependent and androgen receptor-independent mechanisms.

259 ession alterations, and were convergent onto androgen receptor-mediated signaling pathways.

260 and its transcriptional activity through the androgen receptor-STK4/MST1-protein phosphatase 2A axis,

261 tate cancer growth alone and in synergy with androgen-receptor antagonist treatment in vivo.

262 ugh FOXA1, LSD1 inhibition broadly disrupted androgen-receptor binding and its transcriptional output

263 Darolutamide is a structurally distinct androgen-receptor inhibitor that is approved for the tre

264 our results identify ALK5 and non-canonical androgen receptors as potential therapeutic targets for

265 Androgen regulated the differentiation of a unique IL-33

266 e the mechanism by which the steroid hormone androgen regulates YAP1 nuclear entry and functions in s

267 These findings indicate that androgen regulates YAP1 nuclear localization and its tra

268 e activity of testosterone in a cell culture androgen reporter system by competitively displacing tes

269 h and hypothesized that genes with consensus androgen response elements (cAREs) drive proliferation b

270 he miR-146a-5p expression via binding to the Androgen Response Elements on its 5' promoter region, wh

271 PSCC, by co-deletion of Smad4 and Apc in the androgen-responsive epithelium of the penis.

272 neration following castration and subsequent androgen restoration.

273 androgen receptor signaling is necessary for androgen's inactivating effect on phospho-Ser-127 levels

274 longside SSAT upregulation is synergistic in androgen sensitive and castration recurrent CaP models i

275 y co-culture of mouse adipocytes 3T3-L1 with androgen-sensitive LNCaP human prostate cancer cells, or

276 vity, prostate cancer (PCa) cell growth, and androgen sensitivity.

277 ovaries of teleosts, a tissue in which both androgen signaling and zinc dynamics have significant ro

278 Target analysis of hit compounds revealed androgen signaling as a key modulator of ACE2 levels.

279 rovide a better understanding of the role of androgen signaling in neutrophil function and the impact

280 irmed that PRMT5 and pICln both regulate the androgen signaling pathway.

281 d extrinsic genes responsive to Sertoli-cell androgen signaling that promotes cellular states permiss

282 , was rescued by attenuation of oxytocin and androgen signaling, respectively.

283 time to disease progression on the previous androgen signalling-targeted inhibitor, and timing of th

284 y treated with docetaxel and the alternative androgen signalling-targeted inhibitor.

285 rgeted inhibitor, and timing of the previous androgen signalling-targeted inhibitor.

286 e when compared with treatment with a second androgen signalling-targeted inhibitor.

287 ancer with the risk allele gains response to androgen stimulation by recruiting the transcription fac

288 Mechanistically, we find that androgens suppress CDCP1 expression and that androgen de

289 y be used to separate specific effects (e.g. androgen suppression) of individual chemical exposures f

290 l day 4, shortly after a transient perinatal androgen surge in males that could play an organizationa

291 gonize the androgen receptor (AR) or inhibit androgen synthesis in vitro but their potential to cause

292 active concentrations for AR antagonism and androgen synthesis suppression.

293 cation involving CYP17A1, a gene controlling androgen synthesis, and an intrachromosomal inversion in

294 However, the androgens, testosterone and androstenedione were measure

295 istant disease (CRPC) when treated with anti-androgen therapy.

296 ssessment of compounds' effects on estrogen, androgen, thyroid, and PPARgamma receptors of representa

297 me P450 19A1, catalyzes the aromatization of androgens to estrogens within the body.

298 17beta-Estradiol (E2) is produced from androgens via the action of the enzyme aromatase.

299 ish Historic Birth Cohort, in which prenatal androgens were measured, using univariate logistic regre

300 t, 11-ketodihydrotestosterone, are bioactive androgens, with potencies equivalent to those of testost