ライフサイエンスコーパス: androgen

1 in the female degenerate owing to a lack of androgen.

2 critical for generating glucocorticoids and androgens.

3 e differences in response to the presence of androgens.

4 and pregnenolone and is the major source of androgens.

5 enzyme responsible for synthesis of E2 from androgens.

6 omponents in the initiation and evolution of androgen ablation therapy resistance in prostate cancer.

7 prostate cancer progression and relapse post androgen ablation therapy.

8 attention since it is not only resistant to androgen ablation, chemo- and radiotherapy, but also hig

9 proliferation of prostate cancer cells post androgen ablation.

10 rough inhibiting cell proliferation, whereas androgen accelerated tumor growth by promoting cell prol

11 not intraovarian AR actions are key loci of androgen action in generating the PCOS phenotype.

12 This suggests that androgen action promotes metaphyseal corticalization, at

13 re markedly altered, which indicated reduced androgen action.

14 tant (ARKO) mice to investigate the locus of androgen actions that mediate the development of the PCO

15 state cancer cells treated or untreated with androgen after cell-cycle synchronization.

16 r mechanism of action for most existing anti-androgen agents, our findings also raise an interesting

17 , immune checkpoint inhibitors, or even anti-androgens, all of which are being evaluated in phase 1-3

18 the optimal strategy for sequencing between androgen and antiandrogen therapies in metastatic castra

19 The requirement of most prostate cancers for androgen and most breast cancers for estrogen has led to

20 ve methods and develop predictive models for androgen and thyroid pathways.

21 alcohol-associated metabolites, including 7 androgens and alpha-hydroxyisovalerate (OR: 2.23; 95% CI

22 sk, with differences in associations between androgens and histologic subtypes of EOC.

23 idence interval 1.02-1.24); other endogenous androgens and SHBG were not associated with overall risk

24 hat is primarily mediated by the presence of androgens and subsequent mesenchyme-epithelial interacti

25 reclinical results support the importance of androgens and the need for intervention with AR agonists

26 re we find that TSPAN1 is acutely induced by androgens, and is significantly upregulated in prostate

27 ns (estrone, 17beta-estradiol, and estriol), androgens (androstenedione, androsterone, trans-androste

28 The DNA-binding interfaces of the androgen (AR) and glucocorticoid (GR) receptors are virt

29 We measured in vitro estrogen (ER), androgen (AR), and glucocorticoid receptor (GR) activity

30 gy sensor (of 2-OG) that modifies aspects of androgen-AR signalling.

31 mass, function and survival, indicating that androgens are important for extended survival.

32 Androgens are known to protect prostate cancer cells fro

33 ircumventing PI3K-mediated repression of the androgen axis.

34 sociated with the activation of intratumoral androgen biosynthesis and an increase in androgen recept

35 cribe the utility of abiraterone acetate, an androgen biosynthesis inhibitor, in the early treatment

36 ll as Hsd17b3, which encodes a key enzyme in androgen biosynthesis.

37 We found that androgens cause these sex differences by impeding the LT

38 We found that androgen cell-autonomously activates Nkx3.1 expression t

39 Research on prediagnosis androgen concentrations and EOC risk has yielded inconcl

40 ss high levels of AR and retain intratumoral androgen concentrations similar to tumors grown in intac

41 nt (mdx-dm) mice to mimic pre-pubertal nadir androgen condition resulted in premature death, maintena

42 uld promote the proliferation of BECs in low androgen condition via modulation of CCL5/STAT5/CCND1 si

43 city to promote proliferation of BECs in low androgen condition.

44 eity of prostate cancer cells with regard to androgen dependence, defining the character or minor sub

45 tions with three competing cancer "species": androgen dependent, androgen producing, and androgen ind

46 ion of PAGE4 can lead to transitions between androgen-dependent and androgen-independent phenotypes b

47 demonstrate that HIPK1 is expressed in both androgen-dependent and androgen-independent prostate can

48 It occurred in both androgen-dependent and castration-resistant prostate can

49 whereas CLK2 and PAGE4 are expressed only in androgen-dependent cells.

50 of CRPC cells to a greater extent than their androgen-dependent counterparts.

51 mmary tumors, male athymic nude mice bearing androgen-dependent CWR22 prostate cancer xenografts, and

52 ntify kinases that enable tumor formation by androgen-dependent prostate epithelial (LHSR-AR) cells u

53 gand-binding domain (LBD) ensures the strict androgen-dependent regulation of androgen receptor (AR):

54 hese results illuminate a mechanism in which androgen-dependent repression of ERRgamma reprograms pro

55 A genomic variant in the human ADTRP [androgen-dependent tissue factor (TF) pathway inhibitor

56 and highly heritable trait characterized by androgen-dependent, progressive hair loss from the scalp

57 Androgen deprivation (AD) therapy failure leads to termi

58 Correspondingly, androgen deprivation markedly attenuates the frequency a

59 Androgen deprivation or AR inhibition significantly incr

60 tate cancer cells respond heterogeneously to androgen deprivation therapies and reveals characteristi

61 Concordance was greatest for androgen deprivation therapy (ADT) (86.0%, n = 308) alon

62 ing body of evidence supports a link between androgen deprivation therapy (ADT) and cognitive dysfunc

63 ly associated with postoperative response to androgen deprivation therapy (ADT) in a subset analysis

64 e upon androgen receptor (AR) signaling, and androgen deprivation therapy (ADT) is the accepted treat

65 get for adjuvant therapy in combination with androgen deprivation therapy (ADT) to prevent androgen-i

66 c stroke were 1.19 (95% CI, 1.05-1.34) after androgen deprivation therapy (ADT) vs no ADT and 1.21 (9

67 rvational studies have associated the use of androgen deprivation therapy (ADT) with an increased ris

68 g patients with prostate cancer who received androgen deprivation therapy (ADT), after adjustment for

69 The primary end point was androgen deprivation therapy (ADT)-free survival.

70 ate cancer who were initiating or continuing androgen deprivation therapy (ADT).

71 cancer before and 4 wk after treatment with androgen deprivation therapy (ADT).

72 now appears to extend survival compared with androgen deprivation therapy alone.

73 eater than 0.5 ng/mL following radiation and androgen deprivation therapy appears to identify men pri

74 s with advanced prostate cancer treated with androgen deprivation therapy experience relapse with rel

75 stics increasing stroke risk include medical androgen deprivation therapy for ischemic and any stroke

76 Androgen deprivation therapy in the treatment of prostat

77 evaluating the impact on survival of salvage androgen deprivation therapy with or without agents show

78 or radiation therapy followed by 6 months of androgen deprivation therapy, and followed for a median

79 radical prostatectomy, radical radiotherapy, androgen deprivation therapy, and watchful waiting).

80 Despite resistance to initial androgen deprivation therapy, most men respond to second

81 motherapy can improve survival compared with androgen deprivation therapy.

82 oised for selection as dominant clones after androgen deprivation therapy.

83 diation therapy or radiation and 6 months of androgen deprivation therapy.

84 ells of hormonally intact prostate but, upon androgen deprivation, exclusively labels a type of lumin

85 Prostate cancer risk grouping, androgen deprivation, race, age-adjusted CCI, L5HU, and

86 cer (PCa) and its activity can be blocked by androgen-deprivation therapies (ADTs).

87 Twenty-four patients received androgen-deprivation therapy (ADT) and were excluded for

88 ling is a key driver of prostate cancer, and androgen-deprivation therapy (ADT) is a standard treatme

89 ectively randomized clinical trial comparing androgen-deprivation therapy (ADT) plus docetaxel with A

90 Of the 118 patients, 45 were receiving androgen-deprivation therapy (ADT) within at least 6 mo

91 e cancer who have a poor response to initial androgen-deprivation therapy (ADT), as reflected by a pr

92 f this combination in men starting long-term androgen-deprivation therapy (ADT), using a multigroup,

93 are upregulated in prostate cancer following androgen-deprivation therapy (ADT).

94 is characterized by abbreviated response to androgen-deprivation therapy and in approximately 30% of

95 ncer (PCa) differs between those who receive androgen-deprivation therapy by surgical castration and

96 Androgen-deprivation therapy has been identified to indu

97 ly using PARP inhibitors in combination with androgen-deprivation therapy upfront in advanced or high

98 high-risk prostate cancer receiving EBRT and androgen-deprivation therapy, brachytherapy boost (LDR o

99 comorbidities within 1.5 years of initiating androgen-deprivation therapy.

100 s that are poised for clonal selection after androgen-deprivation therapy.

101 cal and molecular properties that respond to androgen-deprivation.

102 nt prostate epithelial (LHSR-AR) cells under androgen-deprived conditions.

103 ases with prostate cancer progression and in androgen-deprived CRPC cells, suggesting that CRPC posse

104 species (ROS), p53 levels and cell death in androgen-deprived CRPC cells.

105 and enzyme activities also were observed in androgen-deprived tumors, consistent with pAKT-dependent

106 ling pathways, pAKT levels were increased in androgen-deprived tumors.

107 Our data suggest TSPAN1 is an androgen-driven contributor to cell survival and motilit

108 of AR with shRNAs and a new generation anti-androgen drug, Enzalutamide, were used to explore the in

109 of gonads and accessory glands attributed to androgen effects, such as testicular atrophy, seminifero

110 Of these 5 androgens, epiandrosterone sulfate (P = 0.0076) was most

111 To study the effects of maternal androgen excess in obese dams on metabolism, placental f

112 Maternal diet-induced obesity, together with androgen excess, affects maternal and fetal liver functi

113 aracteristic; however, it is unclear whether androgen excess, which is treatable, is a cause or a con

114 on, binding events, and motif analyses after androgen exposure identified a metabolic gene expression

115 disorder associated with excess circulating androgens, has been associated with increased risk for a

116 nzyme that is required for the production of androgens, has been exemplified by the approval of abira

117 factors, including imbalances in estrogen or androgen hormones.

118 that the expression of AURKA is regulated by androgen in prostate cancer cells that highly express AR

119 uld be due to diminished anabolic actions of androgens in muscle, and that intervention with an andro

120 that Aurora kinase A (AURKA) is regulated by androgens in prostate cancer cells that express high lev

121 These results implicate androgens in regulating distinct features of complex mot

122 ability in syntax but not phonology, whereas androgens in the robust nucleus of the arcopallium (RA)

123 We show that androgens in two cortex-like vocal control brain regions

124 l subpopulations in prostate cancer that are androgen independent and poised for selection as dominan

125 androgen dependent, androgen producing, and androgen independent.

126 Finally, androgen-independent AR activity in castration-resistant

127 reatment cycles, suppresses proliferation of androgen-independent cells and lowers cumulative drug do

128 rone dosing demonstrate strong selection for androgen-independent cells and rapid treatment failure.

129 ing the character or minor subpopulations of androgen-independent cells that are poised for clonal se

130 ibited expression of AR variants and blocked androgen-independent growth of CRPC cells.

131 rst time that human endostatin (ES) prevents androgen-independent growth phenotype in PCa cells throu

132 e for the retention of male structures in an androgen-independent manner.

133 been shown to block cancer progression in an androgen-independent manner.

134 ect of protumorigenic oxidative machinery on androgen-independent PCa growth, suggesting that ES can

135 o transitions between androgen-dependent and androgen-independent phenotypes by altering the AP-1/and

136 e the antitumor effects of miR-1 and promote androgen-independent proliferation.

137 is expressed in both androgen-dependent and androgen-independent prostate cancer (PCa) cells, wherea

138 Endostatin inhibits androgen-independent prostate cancer growth by suppressi

139 ng, promoting tumor cell survival through an androgen-independent signaling program.

140 ndrogen deprivation therapy (ADT) to prevent androgen-independent tumor cell survival.

141 ine/threonine kinase, NEK6, as a mediator of androgen-independent tumor growth.

142 suggested salT was more predictive than free androgen index (FAI) (p < 0.01).

143 s female pattern hair loss and a higher free androgen index were associated with less wrinkling.

144 We also demonstrate androgen-induced AR binding in the intronic region of AU

145 iferation of mesenchyme cells and suppresses androgen-induced proliferation and differentiation of pr

146 lation of androgen receptor (AR): binding of androgen induces structural reorganization of LBD result

147 ated regulators were compared in tumors from androgen-intact mice and in tumors surviving castration.

148 ndicating that the reduction in intratumoral androgens is a novel mechanism by which antiandrogens me

149 stored in CRPC despite the castrate level of androgens, it is unclear whether AR signaling is signifi

150 e recruited CD8+ T cells on BECs under a low androgen level is still unknown.

151 resulted in premature death, maintenance of androgen levels extended the survival.

152 e the effects of exogenous hormones, such as androgen, luteotropin, and estrogen, on corneal stroma b

153 AR stabilization by androgens makes it distinct from other steroid receptors

154 No androgen marker was more predictive than another using R

155 exacerbation of neurodegenerative processes, androgens may contribute to the epidemiologic sex differ

156 Serum and salivary androgen measurements were determined by LC-MS/MS.

157 As androgens mediate their actions via the androgen recepto

158 nsient over-proliferation, without affecting androgen-mediated luminal cell survival or regeneration.

159 Three other metabolites involved in androgen metabolism, 4-androsten-3beta,17beta-diol disul

160 rosten-3beta,17beta-diol-monosulfate (1), an androgen (OR: 1.61; 95% CI: 1.20, 2.16).

161 peting cancer "species": androgen dependent, androgen producing, and androgen independent.

162 of AMH and steroidogenic genes required for androgen production at day 53 pc.

163 hether chemicals can act together to disrupt androgen production in human fetal testis explants and t

164 of Wolffian ducts was not caused by ectopic androgen production or action.

165 Numerous chemicals are capable of disrupting androgen production, but the possibility that they might

166 Further optimisation of specific androgen-progestin regimens and phase 3 studies of lead

167 e analyzed 33 steroids, including estrogens, androgens, progestins, and glucocorticoids, in hospital

168 evidence for EAF2 as a key factor mediating androgen protection of DNA damage via Ku70/Ku80 in prost

169 Androgen receptor (AR) activation is critical for prosta

170 ens in muscle, and that intervention with an androgen receptor (AR) agonist will reverse musculoskele

171 TSPY and TSPX competitively bind to the androgen receptor (AR) and AR variants, such as AR-V7, a

172 Endogenous TET2 bound the androgen receptor (AR) and AR-coactivator proteins in LN

173 riple-negative breast cancers (TNBC) express androgen receptor (AR) and are potentially responsive to

174 nomously activates Nkx3.1 expression through androgen receptor (AR) binding to the 11-kb region in bo

175 zalutamide (Enz) can occur through bypass of androgen receptor (AR) blockade by the glucocorticoid re

176 Alteration to the expression and activity of androgen receptor (AR) coregulators in prostate cancer i

177 ral androgen biosynthesis and an increase in androgen receptor (AR) expression.

178 igenetically activating transcription of the androgen receptor (AR) in prostate cancer cells.

179 This study investigates the role of androgen receptor (AR) in regulating CXCR7.

180 e of this work was to evaluate the effect of androgen receptor (AR) inhibition on prostate-specific m

181 Androgen receptor (AR) is a transcriptional activator th

182 F-1) domain located in the N-terminus of the androgen receptor (AR) is an attractive therapeutic alte

183 The androgen receptor (AR) is critical for the progression o

184 ighly expressed in cancer cells in which the androgen receptor (AR) is not detected (AR-), whereas th

185 The androgen receptor (AR) is required for prostate cancer (

186 The androgen receptor (AR) is the main driver of prostate ca

187 The androgen receptor (AR) is thought to control the express

188 Androgen receptor (AR) is widely expressed in different

189 Unexpectedly, TRX1 inhibition also elevates androgen receptor (AR) levels under AD, and AR depletion

190 Androgen receptor (AR) mediates the growth of prostate c

191 800 chemicals for estrogen receptor (ER) and androgen receptor (AR) pathway bioactivity.

192 The androgen receptor (AR) pathway is emerging as a potentia

193 d 100 cases of human melanoma and found that androgen receptor (AR) positive melanoma patients have w

194 Here, the authors show that androgen receptor (AR) regulates HR and AR inhibition ac

195 ate cancer (PCa), leading to reactivation of androgen receptor (AR) signaling in a hormone-refractory

196 Androgen receptor (AR) signaling is a distinctive featur

197 Androgen receptor (AR) signaling is a key driver of pros

198 cancer is characterized by a dependence upon androgen receptor (AR) signaling, and androgen deprivati

199 e hormonal treatments due to reactivation of androgen receptor (AR) signaling.

200 imens for prostate cancer focus on targeting androgen receptor (AR) signaling.

201 Androgen receptor (AR) splice variants including AR-V7 f

202 Androgen signals through androgen receptor (AR) to influence prostate development

203 we demonstrate a direct requirement for the androgen receptor (AR) to maintain HR gene expression an

204 ILC2Ps express the androgen receptor (AR), and AR signaling inhibits their

205 As androgens mediate their actions via the androgen receptor (AR), we combined a mouse model of dih

206 drug enzalutamide by a phenotypic shift from androgen receptor (AR)-dependent luminal epithelial cell

207 TEFb (CDK9/cyclin T) plays a central role in androgen receptor (AR)-mediated transactivation by phosp

208 s and lymph node metastasis showing that the androgen receptor (AR)-positive ccRCC may prefer to meta

209 d activation of progenitor genes, as well as androgen receptor (AR)-target genes.

210 cer is driven by androgen stimulation of the androgen receptor (AR).

211 a polyglutamine tract in the gene coding for androgen receptor (AR).

212 h has similar DNA-binding specificity to the androgen receptor (AR).

213 the strict androgen-dependent regulation of androgen receptor (AR): binding of androgen induces stru

214 o those in glucocorticoid receptor (HPA) and androgen receptor (HPG) gene expression.

215 nst MDA-MB-453 cells, a model of the luminal androgen receptor (LAR) subtype of TNBC.

216 activity that is concomitantly modulated by androgen receptor and by CCAAT/enhancer-binding protein

217 fically, we bilaterally implanted the potent androgen receptor antagonist flutamide in two key brain

218 Clinically relevant Ezh2 inhibitors restore androgen receptor expression and sensitivity to antiandr

219 like subtypes were associated with increased androgen receptor expression and signaling, only luminal

220 Here the authors show how androgen receptor expression influences the metastatic r

221 this group, expression of glucocorticoid and androgen receptor genes explained the most variance in t

222 igenic potential of Src and its synergy with androgen receptor in mediating tumor invasion.

223 rase-1 plus androgen receptor is superior to androgen receptor inhibition in metastatic castration-re

224 argeting poly (ADP-ribose) polymerase-1 plus androgen receptor is superior to androgen receptor inhib

225 describes different effects of the selective androgen receptor modulator (SARM) nandrolone phenylprop

226 only 23 (52%) contained 1 or more selective androgen receptor modulators (Ostarine, LGD-4033, or And

227 lty, we describe a novel series of selective androgen receptor modulators (SARMs).

228 Only 52% contained selective androgen receptor modulators and many were inaccurately

229 nalyses of 44 products marketed as selective androgen receptor modulators and sold via the internet,

230 g 44 products marketed and sold as selective androgen receptor modulators, only 23 (52%) contained 1

231 the increasing use of nonsteroidal selective androgen receptor modulators, which have not been approv

232 Products marketed and sold as selective androgen receptor modulators.

233 sers to identify suppliers selling selective androgen receptor modulators.

234 t engagement, evidenced by decreased percent androgen receptor nuclear localization (%ARNL) and incre

235 parg mRNA expression and increased placental androgen receptor protein expression.

236 -independent phenotypes by altering the AP-1/androgen receptor regulatory circuit in PCa cells.

237 n males than in females due to the different androgen receptor signaling but the molecular mechanisms

238 ies showed regulation of DNA repair genes by androgen receptor signaling in prostate cancers.

239 ated with better OS in patients treated with androgen receptor signaling inhibitors (ARSI), whereas h

240 t SPOP mutation activates both PI3K/mTOR and androgen receptor signaling, effectively uncoupling the

241 somatic genomic events in the context of the androgen receptor signaling.

242 We reported previously that the detection of androgen receptor splice variant-7 (AR-V7) mRNA in circu

243 Molecular analyses implicate aberrant androgen receptor stimulation, biliary acid disturbances

244 A-485 inhibited the androgen receptor transcriptional program in both androg

245 e prostate cells, including expansion of the androgen receptor transcriptional repertoire, and ERF ha

246 Androgen receptor variants (AR-Vs) provide a mechanism o

247 ee such master regulators (FOXA1, NKX3.1 and androgen receptor, AR) in a primed conversion strategy s

248 the steroid nuclear hormone receptor family (androgen receptor, estrogen receptor alpha, glucocortico

249 t ERG, through its physical interaction with androgen receptor, induces AR aggregation and endoplasmi

250 ding several haematological malignancies and androgen receptor-positive prostate cancer.

251 We have previously shown that miR-32 is an androgen receptor-regulated miRNA overexpressed in castr

252 Androgen receptor-targeted therapies, including AR agoni

253 itaxel (n = 22); 44.4% received prior potent androgen receptor-targeted therapy.

254 Androgen receptor-targeted treatments for breast cancer

255 strointestinal-lineage genes, independent of androgen-receptor signaling.

256 of cancer-specific transcripts including the androgen-receptor splice variant 7 in a cohort of prosta

257 Notably, these brain regions are rich in androgen receptors and play a key role in modulating agg

258 tein expression levels of AROM, estrogen and androgen receptors did not differ between males and fema

259 ty is repressed by the liganded estrogen and androgen receptors, and by the hypothalamic gonadotropin

260 ive tumours express luminal markers, such as androgen receptors, and have a lower proliferative activ

261 For example, in HVC (proper name), androgens regulate variability in syntax but not phonolo

262 raspanin 1 (TSPAN1) as a clinically relevant androgen regulated target in prostate cancer.

263 ecently identified to be highly sensitive to androgen-regulated AR action, such as NOV and ST6GalNAc1

264 bserved in the expression of certain classic androgen-regulated genes, such as TMPRSS2 and KLK3, desp

265 the fusion of the promoter and 5'-UTR of the androgen-regulated TMPRSS2 (transmembrane protease, seri

266 ELL-associated factor 2 (EAF2) is an androgen-regulated tumor suppressor and its intracellula

267 We find that androgen regulates Sertoli cell phagocytosis by controll

268 ght, suggesting a potential role for EAF2 in androgen regulation of DNA repair in prostate cancer cel

269 In this study, we define NRP1 as an androgen-repressed gene whose expression is elevated dur

270 DNF-repressed gene and Gdnf and Gfralpha1 as androgen-repressed genes in UGS, thus establishing recip

271 Furthermore, EAF2 knockdown blocked androgen repression of LNCaP or C4-2 cells from doxorubi

272 on of alternative lineage programs to bypass androgen requirement.

273 Im) polyamide designed to bind the consensus androgen response element half-site has antitumor activi

274 l luminal cells and CARNs and discovered new androgen response elements in the Nkx3.1 3' UTR.

275 ces miR-185-5p expression via binding to the androgen response elements located on the promoter of mi

276 ion of the endogenous AR target genes in the androgen-responsive LNCaP prostate cancer cells.

277 significantly increased CXCR7 expression in androgen-responsive prostate cancer cell lines, which wa

278 gen receptor transcriptional program in both androgen-sensitive and castration-resistant prostate can

279 How androgen signaling contributes to the oncometabolic stat

280 t, besides blocking AR, antiandrogens modify androgen signaling in CR-VCaP xenografts at multiple lev

281 r song, were also differentially affected by androgen signaling in HVC versus RA.

282 of song were also differentially affected by androgen signaling in HVC versus RA.

283 We show that androgen signaling in the motor cortical-like brain regi

284 Thus, androgen signaling may reduce vocal plasticity by acting

285 stration resistance involves reactivation of androgen signaling or activation of alternative lineage

286 er exhibits a lineage-specific dependence on androgen signaling.

287 Androgen signals through androgen receptor (AR) to influ

288 ticularly strongly associated with decreased androgen steroid metabolites, with all reaching metabolo

289 The expression of AURKA is increased upon androgen stimulation in LNCaP-ARhi cells that express hi

290 Prostate cancer is driven by androgen stimulation of the androgen receptor (AR).

291 preciable level of cellular heterogeneity to androgen stimulation.

292 H) agonists (e.g., triptorelin) are used for androgen suppression therapy.

293 Suppression of androgen synthesis in fetal life has been associated wit

294 at inhibiting AR transcriptional activity or androgen synthesis remains the major mechanism of action

295 during the adaptation of prostate tumors to androgen-targeted therapies (ATTs), and subsequent progr

296 ssociation between pre-diagnosis circulating androgens [testosterone, free testosterone, androstenedi

297 w serum testosterone concentrations (bipolar androgen therapy [BAT]) in this setting might induce tum

298 y the TMPRSS2-ERG gene-fusion, which enables androgens to drive expression of the normally silent E26

299 -label trial exploring the benefit of adding androgens to maintenance therapy in patients 60 years of

300 Androgens, used in the treatment of aplastic anemia, hav