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 ing type I steroid NRs estrogen receptor and progesterone receptor.

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

5 breast cancers express the oestrogen and/or progesterone receptors.

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

7 curred solely by activation of intracellular progesterone receptors.

8 variant, strongly positive for estrogen and progesterone receptors.

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

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

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

12 MetaCore Enrichment analysis identified progesterone receptor action and transforming growth fac

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

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

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

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

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

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

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

20 ng tumor heterogeneity by estrogen receptor, progesterone receptor and human epidermal growth factor

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

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

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

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

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

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

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

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

29 Breast cancer lacking estrogen receptors, progesterone receptors and HER2 receptors are difficult

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

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

32 absence of molecular markers for estrogen or progesterone receptors and human epidermal growth factor

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

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

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

36 of hormone receptors (oestrogen receptor and progesterone receptor) and/or BRCA mutations.

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

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

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

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

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

42 luding those lacking estrogen receptor (ER), progesterone receptor, and HER2 (known as triple-negativ

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

47 ncer subtype lacking estrogen receptor (ER), progesterone receptor, and human epidermal growth factor

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

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

50 ich lacks estrogen receptor alpha (ERalpha), progesterone receptor, and human epidermal growth factor

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

52 s; tumor size; grade; and estrogen receptor, progesterone receptor, and Ki-67 labeling index expressi

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

54 Moreover, progesterone receptor antagonist RU-486 partially revers

55 Progesterone receptor antagonist RU-486 were further app

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

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

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

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

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

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

62 Progesterone receptors are expressed in approximately 70

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

64 Estrogen and progesterone receptors are the established biomarkers th

65 Membrane progesterone receptor as well as classical progesterone

66 Obtained results confirmed how Progesterone-Receptor assay represent a useful tool to s

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

68 his study for the minor allele of rs1042838 (progesterone receptor) (beta = -11.8, 95% confidence int

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

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

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

72 ke kinase 5 (ALK5) in the mouse uterus using progesterone receptor cre ("Alk5 cKO") that develops end

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

74 e EZH2, Ezh2 was conditionally deleted using progesterone receptor Cre recombinase, which is expresse

75 5(d/d)) in the female reproductive organs by progesterone receptor-Cre (Pgr(Cre)) to determine Lgr5's

76 ble-conditional knockout was generated using progesterone receptor-cre (Smad2/3 cKO) mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 t cancer cells characterized by estrogen and progesterone receptor expression (ER+/PR+), to more basa

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

95 ubtypes categorized according to estrogen or progesterone receptor expression and ERBB2 gene amplific

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

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

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

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

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

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

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

103 cT2 to 4b, any N, M0; estrogen receptor and progesterone receptor greater than 50%; human epidermal

104 ore (228; median reduction, 15.0; P = .005), progesterone receptor H-score (15; median reduction, 85.

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

106 xpressed hormone receptors (oestrogen and/or progesterone receptors; HR(+)) but did not have high lev

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

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

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

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

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

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

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

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

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

116 was further tested in oestrogen receptor and progesterone receptor-labelled images.

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

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

119 verexpression of estrogen receptor alpha and progesterone receptor, loss of collagen, increase in pro

120 le-negative breast cancer (estrogen receptor/progesterone receptor < 10%), and five had hormone recep

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

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

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

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

125 uman amnion mesenchymal cells (AMCs) through progesterone receptor membrane component 2 (PGRMC2) and

126 Here we show that progesterone receptor membrane component 2 (PGRMC2) is r

127 Progesterone receptor membrane component-1 (PGRMC1) was

128 igated continuous treatment with a selective progesterone receptor modulator, ulipristal acetate (UPA

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

130 protein-coupled receptors known as membrane progesterone receptors (mPRs).

131 ration in calves, based on quantification of progesterone-Receptor mRNA in bulbo-urethral gland sampl

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

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

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

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

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

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

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

139 specified subgroup analyses in patients with progesterone receptor-negative disease; patients with a

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

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

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

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

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

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

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

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

148 natural and synthetic ligands of the nuclear progesterone receptor (nPR) has been pointed out, howeve

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

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

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

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

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

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

155 well as gain of PTK6 and the membrane-bound progesterone receptor, PAQR8.

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

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

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

159 Progesterone receptor (PGR) co-ordinately regulates ovul

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

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

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

163 ifferences in the relative abundances of the progesterone receptor (PGR) isoforms PGRA and PGRB are o

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

165 For example, we find that Progesterone Receptor (PGR) phosphorylation is associate

166 e found that alterations in progesterone and progesterone receptor (Pgr) signalling strongly suppress

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

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

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

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

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

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

173 95% CI: 1.20, 4.67; P-heterogeneity with ER+/progesterone receptor positive = 0.06).

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

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

176 2 of 3, that was estrogen receptor positive, progesterone receptor positive, and HER2 negative.

177 ive ductal carcinomas that were estrogen and progesterone receptor-positive (ER/PR+) and HER2/neu-neg

178 % confidence interval (CI): 1.19, 1.83); for progesterone receptor-positive (PR+) cancer, 1.64 (95% C

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

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

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

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

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

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

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

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

187 ts suggest that MPA is efficient in treating progesterone receptor-positive CIN lesions.

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

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

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

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

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

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

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

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

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

197 ), 0.90 for estrogen receptor (ER) -positive progesterone receptor (PR) -positive breast cancer (95%

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

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

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

201 n of the steroid has a significant impact on progesterone receptor (PR) and androgen receptor (AR) ac

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

203 major receptors i.e. estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth fa

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

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

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

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

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

209 Progesterone receptor (PR) and progestins affect mammary

210 e have identified an interaction between the progesterone receptor (PR) and STAT1 in breast cancer ce

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

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

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

214 Estrogen receptor (ER) and progesterone receptor (PR) are important prognostic and

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

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

217 Since progesterone and the progesterone receptor (PR) can activate many GREs, we hy

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

219 The progesterone receptor (PR) controls female sexual behavi

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

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

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

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

224 T/CT imaging of tumor glucose metabolism and progesterone receptor (PR) expression, respectively.

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

226 -6(f/f) mice and decreased expression of the progesterone receptor (PR) in stromal cells.

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

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

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

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

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

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

233 Ulipristal acetate (UPA) a selective progesterone receptor (PR) modulator (SPRM) reduce the s

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

235 Progesterone receptor (PR) positive stromal cells transc

236 ha) reactivity, but have decreased levels of progesterone receptor (PR) protein.

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

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

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

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

241 We now demonstrate that progesterone and the progesterone receptor (PR) stimulate productive infectio

242 ER and progesterone receptor (PR) were significantly lower in m

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 Estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth f

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

247 t cancer risk and by estrogen receptor (ER), 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 ms whereby progesterone (P4), acting via the progesterone receptor (PR), inhibits proinflammatory/con

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

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

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

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

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

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

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

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

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

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

261 ve cells), and MCF-7 (estrogen receptor (ER)/progesterone receptor (PR)-positive cell line) with negl

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

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

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

265 resulting from its ability to antagonize the progesterone receptor (PR).

266 one receptor antagonists (ER/ICI 182,780, or progesterone receptor (PR)/ RU486) for 48 h.

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

268 Progesterone receptors (PR) are transcription factors re

269 We find that progesterone-receptor (PR)-expressing neurons in the ven

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

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

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

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

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

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

276 ury was not associated with child cognition, progesterone receptor rs1042838 minor alleles revealed a

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

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

279 0.0001), high tumor grade, negative estrogen/progesterone receptor status, and human epidermal growth

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

281 ncomplete data on oestrogen receptor status, progesterone receptor status, or HER2 status were exclud

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

283 history of CNS metastases, and oestrogen and progesterone receptor status.

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

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

286 e with mutations in the nuclear estrogen and progesterone receptors, suggesting a role in treatment r

287 The expression of progesterone receptor target genes including the Indian

288 An inhibitor of the non-genomic progesterone receptor that activates CatSper similarly b

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

290 Confirming the role of the progesterone receptor, the preventive effect of MPA was

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

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

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

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

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

296 s transgenic mice in which the expression of progesterone receptor was genetically ablated.

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

300 iptional programs controlled by estrogen and progesterone receptors, without fully abrogating them.