ライフサイエンスコーパス: progesterone receptor

1 nhibitors), and steroidogenesis (CYP21A2 and progesterone receptor).

2 mmunohistochemistry for ERalpha, ERbeta, and progesterone receptor.

3 ion of the estrogen responsive genes pS2 and progesterone receptor.

4 ing type I steroid NRs estrogen receptor and progesterone receptor.

5 coid receptor, and partial antagonism of the progesterone receptor.

6 iated by a specialized, non-genomic membrane progesterone receptor.

7 sive genes including pS2, complement C3, and progesterone receptor.

8 e the two based on staining for estrogen and progesterone receptors.

9 variant, strongly positive for estrogen and progesterone receptors.

10 curred solely by activation of intracellular progesterone receptors.

11 pes as defined by the status of estrogen and progesterone receptors.

12 Invasive tumors overexpress the short progesterone receptor A (PR-A) isoform.

13 nthase kinase (GSK)-3beta phosphorylation of progesterone receptor-A (PR-A) facilitates its ubiquitin

14 he discovery by mass spectrometry of a novel progesterone receptor acetylation site at Lys-183 that i

15 mammary gland development, Her2 activation, progesterone receptor activity, prolactin effects, and a

16 modulation of androgen, glucocorticoid, and progesterone receptor activity.

17 Devoid of the estrogen and progesterone receptors, along with the receptor tyrosine

18 ene and grade and negatively correlated with progesterone receptor and estrogen receptor.

19 ot express the genes for oestrogen receptor, progesterone receptor and HER2 (also called ERBB2 or NEU

20 formed were negative for estrogen receptor, progesterone receptor and HER2.

21 mors typically lack estrogen receptor-alpha, progesterone receptor and HER2/ERBB2, or in other words

22 cluding tumour size and grade; oestrogen and progesterone receptor and human epidural growth factor r

23 metabolic analyses to study the role of the progesterone receptor and its transcriptional regulator,

24 nger RNA levels for estrogen receptor-alpha, progesterone receptor and smooth muscle cell markers wer

25 The identity of this non-genomic progesterone receptor and the mechanism by which it caus

26 cers positive for both estrogen receptor and progesterone receptor and those that were negative for h

27 tumors that by definition lack estrogen and progesterone receptors and amplification of the HER2 gen

28 negative breast cancer lacking oestrogen and progesterone receptors and ERBB2 expression.

29 regulates the androgen, glucocorticoid, and progesterone receptors and has no effect on the mineralo

30 e breast cancers (TNBC) lacking estrogen and progesterone receptors and HER2 amplification have a rel

31 I or III breast cancers lacking estrogen and progesterone receptors and HER2/Neu (TNBC) were enrolled

32 mor is triple negative, lacking estrogen and progesterone receptors and human epidermal growth factor

33 In addition to estrogen and progesterone receptors and human epidermal growth factor

34 arcinoma, strongly positive for estrogen and progesterone receptors and negative for human epidermal

35 of breast cancer (negative for estrogen and progesterone receptors and v-erb-b2 avian erythroblastic

36 id receptor, mineralocorticoid receptor, and progesterone receptor) and their endogenous ligands.

37 positive family history, estrogen receptor+, progesterone receptor+, and/or human epidermal growth fa

38 ng staining for the estrogen receptor alpha, progesterone receptor, and c-erbB-2.

39 iption of the estrogen-responsive genes pS2, progesterone receptor, and cyclin D1.

40 sion, and biomarkers (eg, estrogen receptor, progesterone receptor, and epidermal growth factor recep

41 ers that are negative for estrogen receptor, progesterone receptor, and ERBB2 (triple-negative breast

42 defined by the absence of estrogen receptor, progesterone receptor, and HER-2 expression, account for

43 to use preferentially the estrogen receptor, progesterone receptor, and HER2 status of the metastasis

44 process and retesting of estrogen receptor, progesterone receptor, and HER2 status should be offered

45 triple-negative breast cancer (negative ER, progesterone receptor, and HER2).

46 pe defined by the lack of estrogen receptor, progesterone receptor, and human epidermal growth factor

47 scheme, which is based on estrogen receptor, progesterone receptor, and human epidermal growth factor

48 -negative (TN) phenotype (estrogen receptor, progesterone receptor, and human epidermal growth factor

49 No biomarker except for estrogen receptor, progesterone receptor, and human epidermal growth factor

50 tumor size and grade, and estrogen receptor, progesterone receptor, and Ki-67 expression levels.

51 e PTBs induced by bacterial endotoxin LPS or progesterone receptor antagonist mifepristone more often

52 Moreover, progesterone receptor antagonist RU-486 partially revers

53 Progesterone receptor antagonist RU-486 were further app

54 Where labor was induced using the progesterone receptor antagonist RU486, NFkB and AP-1/JN

55 horylation were independent of the classical progesterone receptor antagonist RU486.

56 However, microinjection of the progesterone receptor antagonist, RU486, into the AVPV r

57 t express estrogen receptor-alpha (Esr1) and progesterone receptor are essential for male but not fem

58 ee energies for three ligands binding to the progesterone receptor are in very good agreement with ex

59 st cancer in which the estrogen receptor and progesterone receptor are not expressed, and human epide

60 Progesterone receptors are expressed in approximately 70

61 Previously, we reported that the progesterone receptors are stabilized in Brca1-deficient

62 Membrane progesterone receptor as well as classical progesterone

63 ers, hyperactive Akt signaling downregulates progesterone receptor B (PRB) transcriptional activity,

64 ferences were detected in estrogen receptor, progesterone receptor, beta-catenin, or vimentin express

65 induction by progesterone is mediated by two progesterone receptor-binding elements in the intron reg

66 3) A tendency for decreased expression of progesterone receptor co-activators (NCOA1, -2 and -3, a

67 l and in the neonatal mouse uterus using the progesterone receptor Cre (Pgr-Cre) model.

68 5(d/d)) in the female reproductive organs by progesterone receptor-Cre (Pgr(Cre)) to determine Lgr5's

69 we conditionally ablated uterine ALK5 using progesterone receptor-cre mice to define the physiologic

70 al knockout (cKO) of Fst in the uterus using progesterone receptor-cre to study the roles of uterine

71 ted a conditional knockout mouse model using progesterone receptor-Cre-recombinase to achieve Pten an

72 In accord with these phenotypic changes, progesterone receptor, cyclin D1, and Mmp2 were up-regul

73 t work on the risk of estrogen receptor- and progesterone receptor-defined breast cancers was evaluat

74 our-cell density involving microRNA-mediated progesterone receptor downregulation, and was reversible

75 Study stratifiers were estrogen receptor/progesterone receptor (ER/PgR), human epidermal growth f

76 by the expression status of the estrogen and progesterone receptors (ER and PR) and human epidermal g

77 primary human MCs lack classical estrogen or progesterone receptors (ER or PR).

78 (TNBC) that lack expression of estrogen and progesterone receptors (ER/PR), or amplification or over

79 ast cancer that is negative for estrogen and progesterone receptors (ER/PR-negative).

80 biomarkers, such as, estrogen receptor-alpha/progesterone receptor (ERalpha/PR), predict only slightl

81 nk between the PRLr TAD and the estrogen and progesterone receptors (ERalpha/PR).

82 induced by 3-ketosteroids lacked ERalpha and progesterone receptors, expressed stem cell marker, CD44

83 ression revealed that PNA mice had 59% fewer progesterone receptor-expressing cells in the arcuate nu

84 A recent study identifies progesterone receptor-expressing neurons in the hypothal

85 r estrogen receptor expression (90%) and for progesterone receptor expression (40%) and had a Ki-67 s

86 alpha (rho = 0.65, P < 0.01) and weakly with progesterone receptor expression (rho = 0.46, P = 0.03)

87 tumor was strongly positive for estrogen and progesterone receptor expression and had a Ki-67 score o

88 mical analysis was positive for estrogen and progesterone receptor expression and negative for human

89 gland development through direct effects on progesterone receptor expression and pathways regulated

90 ) - defined by lack of estrogen receptor and progesterone receptor expression as well as lack of huma

91 ession in patients lacking estrogen receptor/progesterone receptor expression in their breast tissue.

92 D3 also affected uterine progesterone receptor expression patterns similar to E2.

93 was positively correlated with oestrogen and progesterone receptor expression whereas BUB1B was negat

94 low histological grade and with estrogen and progesterone receptor expression, accordant with inducti

95 ogen receptor expression (50%), negative for progesterone receptor expression, and had a Ki-67 score

96 Here we report that cyclin D1 regulates progesterone receptor expression, consequently enhancing

97 In vivo, association of Reptin with the progesterone receptor gene promoter is concomitant with

98 Classic estrogen-induced regulation of the progesterone receptor gene was demonstrated by increased

99 ability to modulate expression of the human progesterone receptor gene.

100 for how factors such as oestrogen receptor, progesterone receptor, HER2, and indicators of prolifera

101 IHC analysis of estrogen receptor, progesterone receptor, human epidermal growth factor rec

102 d from immunohistochemical assessment of ER, progesterone receptor, human epidermal growth factor rec

103 howed significantly less colocalization with progesterone receptor in PNA animals compared with contr

104 C) nuclei, while the region-specific role of progesterone receptors in these nuclei remains unknown.

105 ant recurrence, but the status regarding the progesterone receptor (in 54,115 patients) and human epi

106 Here, we report that progesterone receptor inhibits cervical and vaginal epit

107 To further explore how the stability of progesterone receptor is modulated, here, we have found

108 Given that the CatSper-associated progesterone receptor is sperm specific and structurally

109 Our data suggest that Cripto-1, like the progesterone receptor, is not required for the initial d

110 and structurally different from the genomic progesterone receptor, it represents a promising target

111 histopathologic markers (estrogen receptor, progesterone receptor, Ki-67, human epidermal growth fac

112 Progesterone receptor levels decreased in cyclin D1 knoc

113 Lower estrogen and progesterone receptor levels in LMSP suggests an indirec

114 although they have remarkably lower estrogen/progesterone receptor levels than mature myometrial or l

115 Intestine-restricted activation of membrane progesterone receptors may represent a novel approach fo

116 n in vitro organ culture system to show that progesterone receptor membrane component 1 (PGRMC1) medi

117 eceptor binding site is localized within the progesterone receptor membrane component 1 (PGRMC1), mos

118 S2R (sigma-2 receptor)/Pgrmc1 (progesterone receptor membrane component 1) is a cytochr

119 rane-bound protein was identified as PGRMC1 (progesterone receptor membrane component 1).

120 Progesterone receptor membrane component-1 (PGRMC1) was

121 morphology in women exposed to asoprisnil, a progesterone receptor modulator.

122 receptor alpha, estrogen receptor beta, and progesterone receptor mRNA and protein throughout the te

123 positive (OR, 5.17; 95% CI, 1.64 to 17.01), progesterone receptor negative (OR, 2.63; 95% CI, 1.58 t

124 estrogen receptor moderately positive (60%), progesterone receptor negative and Her2-neu that is not

125 negative, estrogen receptor positive (80%), progesterone receptor negative, and human epidermal grow

126 e negative" (ie, estrogen receptor negative, progesterone receptor negative, and human epidermal grow

127 Women with estrogen receptor- and progesterone receptor-negative (< 10% positive cells by

128 n was greater for estrogen receptor-negative progesterone receptor-negative (ER-PR-) tumors (RR: 0.66

129 observed for estrogen receptor-negative and progesterone receptor-negative (HR(Q5-Q1):0.74; 95% CI:

130 HER2+) tumors and triple-negative (TN) (ER-, progesterone receptor-negative (PR-) and normal HER2) tu

131 JNK activity and are significantly higher in progesterone receptor-negative and HER2-positive breast

132 ated with risk of estrogen receptor-negative/progesterone receptor-negative breast cancer, and that s

133 breast cancer but not estrogen receptor- and progesterone receptor-negative disease.

134 des, worse grade, and estrogen receptor- and progesterone receptor-negative status) were associated w

135 cer was found for retinol in relation to ER-/progesterone receptor-negative tumors (OR: 2.37; 95% CI:

136 n between progesterone receptor-positive and progesterone receptor-negative tumors in postmenopausal

137 irmed estrogen receptor (ER)-positive (90%), progesterone receptor-negative, HER2-negative recurrent

138 sided, T2N1, grade 3, estrogen receptor- and progesterone receptor-negative, human epidermal growth f

139 tive tissue-rich, and estrogen receptor (ER)/progesterone receptor-negative.

140 vs hormone receptor-negative [oestrogen and progesterone receptor-negative]), nodal status (0, 1-3,

141 ancer and 63% for estrogen receptor-negative progesterone- receptor-negative cancer.

142 ed protein serves as the elusive non-genomic progesterone receptor of sperm.

143 id not vary based on age, estrogen receptor, progesterone receptor, or HER2 status.

144 h low or no expression of estrogen receptor, progesterone receptor, or human epidermal growth factor

145 BC does not express estrogen receptor-alpha, progesterone receptor, or the HER2 oncogene; therefore,

146 Using progesterone receptor- or Hmox1-deficient mice, we ident

147 r (TNBC), as compared to estrogen receptor-, progesterone receptor- or human epidermal growth factor

148 th higher percentages of estrogen receptor-, progesterone receptor-, or ki67-positive mammary epithel

149 Knockdown of the membrane progesterone receptors Paqr5 or Paqr7 in GLUTag cells el

150 N1ICD) in the reproductive tract driven by a progesterone receptor (Pgr) -Cre.

151 ble gene 6 (Mig-6) is a critical mediator of progesterone receptor (PGR) action in the uterus.

152 says of 1) HER2 and estrogen receptor and 2) progesterone receptor (PgR) and p53 were performed on th

153 y the expression of amphiregulin (Areg), the progesterone receptor (Pgr) and signal transducer and ac

154 correlates with estrogen receptor (ER+) and progesterone receptor (PGR) expression and longer progre

155 ogy substudy testing the predictive value of progesterone receptor (PgR) expression for outcome of es

156 tivity, and estrogen receptor (ER) regulated progesterone receptor (PgR) gene expression.

157 tor (AR), ERalpha (ESR1), ERbeta (ESR2), and progesterone receptor (PGR) genes.

158 The progesterone receptor (PGR) is a ligand-activated transc

159 Immunohistochemical analysis for ER and progesterone receptor (PgR) percentage expression (46 su

160 Centrally reviewed estrogen receptor (ER), progesterone receptor (PgR), and HER2 copy numbers were

161 status, tumor size, estrogen receptor (ER), progesterone receptor (PgR), human epidermal growth fact

162 r (Gr), mineralocorticoid receptor (Mr), and progesterone receptor (Pgr)] with sets of steroid target

163 clinically relevant subclasses: (i) estrogen/progesterone receptor positive (ER+/PR+), (ii) HER2/ERRB

164 st cancers were diagnosed [3479 estrogen and progesterone receptor positive (ER+PR+); 1021 ER and PR

165 Reported proportions of ER positive (ER+), progesterone receptor positive (PR+), and human epiderma

166 95% CI: 1.20, 4.67; P-heterogeneity with ER+/progesterone receptor positive = 0.06).

167 mone receptor status (oestrogen receptor and progesterone receptor positive vs others), and region.

168 re estrogen receptor positive, 67 (80%) were progesterone receptor positive, and 19 (23%) were human

169 2 of 3, that was estrogen receptor positive, progesterone receptor positive, and HER2 negative.

170 % confidence interval (CI): 1.19, 1.83); for progesterone receptor-positive (PR+) cancer, 1.64 (95% C

171 in the appearance of estrogen receptor- and progesterone receptor-positive and ErbB2-negative infilt

172 nt heterogeneity (P = 0.05) was seen between progesterone receptor-positive and progesterone receptor

173 sociated with risk of estrogen receptor- and progesterone receptor-positive breast cancer but not est

174 HER2-positive and estrogen receptor-positive/progesterone receptor-positive breast cancer, clinicians

175 with risk for estrogen receptor-positive and progesterone receptor-positive breast cancers (HR, 1.86;

176 is linked to poor prognosis in estrogen and progesterone receptor-positive breast cancers.

177 , we examined estrogen receptor-positive and progesterone receptor-positive breast tumors from five p

178 oid reexcision in estrogen receptor-positive progesterone receptor-positive cancer and 63% for estrog

179 patients with estrogen receptor-negative and progesterone receptor-positive cancer).

180 bserved between consecutive night shifts and progesterone receptor-positive cancers suggests that pro

181 The number of estrogen- and progesterone receptor-positive cells, as well as the exp

182 d a PS of 0 (88%), had estrogen receptor and progesterone receptor-positive disease (52%), had one to

183 mone agonist, with estrogen receptor- and/or progesterone receptor-positive disease at first relapse

184 ume and slowly progressive estrogen receptor/progesterone receptor-positive disease, antiestrogen the

185 mor epithelia from estrogen receptor- and/or progesterone receptor-positive human epidermal growth fa

186 tus (hormone receptor-positive [oestrogen or progesterone receptor-positive or both] vs hormone recep

187 .01) than for estrogen receptor-positive and progesterone receptor-positive tumors (0.92: 0.81, 1.03;

188 t shifts, with the highest risk observed for progesterone receptor-positive tumors (odds ratio = 2.4,

189 increased risk of estrogen receptor-positive progesterone receptor-positive tumors (RR: 1.29; 95% CI:

190 Estrogen and/or progesterone receptor-positive tumors displayed more hyp

191 lly confirmed oestrogen receptor-positive or progesterone receptor-positive, or both, locally advance

192 On multivariate analysis, patient age and progesterone receptor positivity of the index cancer wer

193 atory breast cancer, and by oestrogen and/or progesterone receptor positivity.

194 ), 0.90 for estrogen receptor (ER) -positive progesterone receptor (PR) -positive breast cancer (95%

195 Optimal cutoffs of percentage of progesterone receptor (PR) -positive tumor cells to pred

196 s revealed that Lys-183 is a primary site of progesterone receptor (PR) acetylation.

197 terine quiescence is maintained by increased progesterone receptor (PR) activity, but labor is facili

198 whether cytoplasmic interactions between the progesterone receptor (PR) and estrogen receptor alpha (

199 Each imaging finding, progesterone receptor (PR) and human epidermal growth fa

200 cedes implantation is directly controlled by progesterone receptor (PR) and is independent of VEGF.

201 TA-binding protein (TBP) with the NTD of the progesterone receptor (PR) and its ability to regulate A

202 Progesterone acting through the progesterone receptor (PR) and its coregulators prepares

203 We examined whether tumour expression of the progesterone receptor (PR) and oestrogen receptor (ER) w

204 Progesterone receptor (PR) and progestins affect mammary

205 xpression of the estrogen receptor (ER), the progesterone receptor (PR) and the ERBB2 (also known as

206 functional P4 withdrawal, reflecting reduced progesterone receptor (PR) and/or glucocorticoid recepto

207 Estrogen receptor-alpha (ERalpha) and progesterone receptor (PR) are expressed in most human b

208 Estrogen receptor alpha (ERalpha) and progesterone receptor (PR) are important steroid hormone

209 improving the selectivity for MR versus the progesterone receptor (PR) as an approach to avoid poten

210 defined by cancer estrogen receptor (ER) and progesterone receptor (PR) content, and HER2 content (hu

211 The progesterone receptor (PR) controls female sexual behavi

212 , we probed estrogen receptor-alpha (ER) and progesterone receptor (PR) cross-talk in breast cancer m

213 Progesterone receptor (PR) exists in two isoforms, PRA a

214 pausal status and estrogen receptor (ER) and progesterone receptor (PR) expression in tumors.

215 FGFR1 signaling suppresses progesterone receptor (PR) expression in vitro, and like

216 Progesterone receptor (PR) expression is used as a bioma

217 Conjugates targeting the promoter of the progesterone receptor (PR) function as antigene agents t

218 ndidate miRNAs predicted to target the human progesterone receptor (PR) gene promoter were tested for

219 1-4 in gene silencing and activation of the progesterone receptor (PR) gene.

220 We present here the x-ray structures of the progesterone receptor (PR) in complex with two mixed pro

221 The roles of progesterone (P(4)) and of progesterone receptor (PR) in development and pathogenes

222 -6(f/f) mice and decreased expression of the progesterone receptor (PR) in stromal cells.

223 quired for decidualization, interacting with progesterone receptor (PR) in uterus.

224 , suggesting that reduced reproductive-tract progesterone receptor (PR) initiates labor.

225 Progesterone receptor (PR) is a master regulator in fema

226 Furthermore, we find that while nuclear progesterone receptor (PR) is liganded during human preg

227 Progesterone receptor (PR) is usually co-localized with

228 collective term for endogenous and synthetic progesterone receptor (PR) ligands.

229 that was estrogen receptor (ER) positive and progesterone receptor (PR) negative and lacked amplifica

230 Progesterone receptor (PR) positive stromal cells transc

231 were approximated: estrogen receptor (ER) or progesterone receptor (PR) positive, HER2 negative, and

232 = .002), and negative estrogen receptor (ER)/progesterone receptor (PR) status (P < .001/P < .001).

233 breast cancer by estrogen receptor (ER) and progesterone receptor (PR) status are limited.

234 ggested that when estrogen receptor (ER) and progesterone receptor (PR) status are mutually considere

235 cancer defined by estrogen receptor (ER) and progesterone receptor (PR) status are not well understoo

236 Further stratification by progesterone receptor (PR) status showed slightly strong

237 histological type and estrogen receptor (ER)/progesterone receptor (PR) status were calculated with s

238 based measures of estrogen receptor (ER) and progesterone receptor (PR) status were compared with imm

239 sion (L), estrogen receptor (ER) status (E), progesterone receptor (PR) status, combined ER and PR st

240 pausal status and estrogen receptor (ER) and progesterone receptor (PR) status.

241 ) alpha-, beta-, or G-protein-coupled ER1 or progesterone receptor (PR) substantially reduces KOR/MOR

242 r alpha (ERalpha)+ MECs, but only rare (<1%) progesterone receptor (PR)+ and RANKL+ cells.

243 also led to reduced expression of the ER and progesterone receptor (PR), and diminished responsivenes

244 re used to determine estrogen receptor (ER), progesterone receptor (PR), and HER2 status, which was t

245 sh women with known oestrogen receptor (ER), progesterone receptor (PR), and HER2 statuses, and 360 c

246 subtypes, defined by estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth f

247 ssion of estrogen receptor-alpha (ER-alpha), progesterone receptor (PR), and human epidermal growth f

248 Progesterone, an agonist for the progesterone receptor (PR), can be an efficacious and we

249 ian steroid progesterone, acting through the progesterone receptor (PR), coordinates endometrial epit

250 ght to determine whether risks differ by ER, progesterone receptor (PR), human epidermal growth facto

251 ms whereby progesterone (P4), acting via the progesterone receptor (PR), inhibits proinflammatory/con

252 tion factor SMAD family member 4 (SMAD4) and progesterone receptor (PR), is necessary to inhibit uter

253 expression and activity of ER-alpha and the progesterone receptor (PR), MEL-18 overexpression restor

254 r (ER)-positive breast cancers coexpress the progesterone receptor (PR), which can directly and globa

255 duced Dgcr8 conditional knock-out mice using progesterone receptor (PR)-Cre (Dgcr8(d/d)) and demonstr

256 Furthermore, a progesterone receptor (PR)-Cre Notch1 bigenic (Notch1(d/

257 ry cues, social context, and sex hormones on progesterone receptor (PR)-expressing neurons in the ven

258 re "triple-negative" [estrogen receptor (ER)-progesterone receptor (PR)-HER2+; n = 19].

259 ly those with larger (Pinteraction = 0.036), progesterone receptor (PR)-negative (Pinteraction < 0.00

260 ssociated with triple-negative (ER-negative, progesterone receptor (PR)-negative and human epidermal

261 ncreased risk of estrogen receptor (ER)- and progesterone receptor (PR)-negative tumors in women age

262 s within luminal estrogen receptor (ER)- and progesterone receptor (PR)-positive breast cancers.

263 cancer cells in estrogen receptor (ER)- and progesterone receptor (PR)-positive breast tumors.

264 in response rate for estrogen receptor (ER)/progesterone receptor (PR)-positive tumors were found, b

265 RUNX1 was associated with progesterone receptor (PR)-positive tumours (P<0.05), mo

266 r (GR), mineralocorticoid receptor (MR), and progesterone receptor (PR).

267 s also displayed increased expression of the progesterone receptor (PR).

268 Here we investigated the mechanisms by which progesterone receptors (PR) and retinoic acid receptors

269 Progesterone receptors (PR) are critical mediators of ma

270 Progesterone receptors (PR) are transcription factors re

271 st cancer (oestrogen receptor [ER] positive, progesterone receptor [PR] positive, or both) were eligi

272 r five nevi, 1.09, 95% CI, 1.02-1.16 for ER+/progesterone receptor [PR]-positive tumors; 1.08, 95% CI

273 P), as well the feasibility of imaging tumor progesterone receptors (PRs) by PET in breast cancer.

274 one, acting in large measure through nuclear progesterone receptors (PRs) in uterine and cervical tis

275 Progesterone receptors (PRs), which mediate the cellular

276 rodents, estrogens induce the expression of progesterone receptors (PRs).

277 f breast cancer usually lacking estrogen and progesterone receptors, remains difficult to treat.

278 oid receptor family (estrogen, androgen, and progesterone receptors) reveals variation in oligomeriza

279 ve regulator of androgen, glucocorticoid and progesterone receptor signaling pathways.

280 ed by age, axillary nodes, and oestrogen and progesterone receptor status and randomly assigned in a

281 tients with luminal B tumors irrespective of progesterone receptor status or baseline Ki-67 expressio

282 e at diagnosis, estrogen receptor status and progesterone receptor status) as joint determinants of B

283 0.0001), high tumor grade, negative estrogen/progesterone receptor status, and human epidermal growth

284 presence of multifocal disease, estrogen and progesterone receptor status, HER2/neu status, presence

285 ardless of tumor grade and size, estrogen or progesterone receptor status, human epidermal growth fac

286 e interval (CI), 0.94-1.39], by estrogen and progesterone receptor status, or by ages at first-term b

287 measureable lesion; and known oestrogen and progesterone receptor status.

288 revious chemotherapy, oestrogen-receptor and progesterone-receptor status, and location of ILRR.

289 core biopsy reveals IDC that is estrogen and progesterone receptor strongly positive (> 90%) and Her2

290 The expression of progesterone receptor target genes including the Indian

291 present characterization of the human sperm progesterone receptor that is conveyed by the orphan enz

292 which do not express the HER2, estrogen, and progesterone receptors) through novel receptors, harness

293 e progesterone receptor as well as classical progesterone receptor trafficked to the membrane mediate

294 r receptor 2 (HER2) and the estrogen and the progesterone receptors (triple negative; TNBC) are more

295 ncoded by the MKI67 gene, estrogen receptor, progesterone receptor, tumor size, and RS were univariat

296 hotspot, directly upstream of the well-known progesterone receptor tumour suppressor pathway.

297 Neither estrogen receptor alpha nor progesterone receptor were detected in lymphatic endothe

298 ed through an interaction between SMTNL1 and progesterone receptor, which alters the expression of co

299 ed expression of estrogen receptor alpha and progesterone receptor, which is common in advanced stage

300 ha is known to up-regulate expression of the progesterone receptor, which, on activation by its ligan