ライフサイエンスコーパス: progestin

1 mone therapy used (estrogen vs estrogen plus progestin).

2 strogen alone or an estrogen combined with a progestin.

3 t at this site in the absence or presence of progestin.

4 group randomized to E-alone or estrogen plus progestin.

5 risk of taking HT, especially estrogen plus progestin.

6 eved with a combination of an androgen and a progestin.

7 increased with combined use of estrogen plus progestin.

8 en only in colonies or tumors treated with a progestin.

9 those previously reported for estrogen plus progestin.

10 nalyses are also presented for estrogen plus progestin.

11 mmunomodulatory properties of this exogenous progestin.

12 lacking for altrenogest, a potent synthetic progestin.

13 nation HTs, which include both estrogens and progestins.

14 nity exists for progesterone and its related progestins.

15 for maximal induction of E2F1 expression by progestins.

16 indings may include unanticipated effects of progestins.

17 r relative affinity than reference steroidal progestins.

18 anyl, phenyl, and thiophenyl aldehydes and a progestin 16alpha,17alpha,21-triol (5) in the presence o

19 catalyzes the biosynthesis of androgens from progestins, 3beta-(hydroxy)-17-(1H-benzimidazole-1-yl)an

20 usions of U73122 (400nM/side), should reduce progestin (5alpha-pregnan-3alpha-ol-20-one; 3alpha,5alph

21 ransgenic animals were highly susceptible to progestin/7,12-dimethylbenz(a)anthracene-induced mammary

22 o receive a human therapeutic dose for these progestins according to modeled bioconcentration factors

23 cyte maturation in teleosts by estrogens and progestins acting through GPER and mPRalpha, respectivel

24 If progestins' actions through D1 and GABA(A) receptors in

25 Progesterone receptor (PR) and progestins affect mammary tumorigenesis; however, the re

26 eduction in attack frequency was 99.8% under progestins after discontinuing eOC (16 women), 93.8% und

27 d, placebo-controlled trial of estrogen plus progestin, after a mean intervention time of 5.6 (SD, 1.

28 Tanaproget is a nonsteroidal progestin agonist with very high PR binding affinity and

29 The synthetic progestins also masculinized the female fish in a concen

30 Around 20 progestins (also called gestagens, progestogens, or prog

31 Progestins alter hormone homeostasis and may result in r

32 Gestodene is a human contraceptive progestin and a potent activator of fish androgen recept

33 The progestin and AdipoQ receptor (PAQR) family of proteins

34 Proteins belonging to the Progestin and AdipoQ Receptor (PAQR) superfamily of memb

35 erevisiae belongs to the newly characterized progestin and adipoQ receptor (PAQR) superfamily of rece

36 rotein-coupled estrogen receptor (GPER), and progestin and adipoQ receptor 7 (PAQR7).

37 et al. provide evidence that, in yeast, the progestin and adipoQ receptor superfamily of receptors m

38 ee exponent gamma=2.3), which suggested that progestin and corticosteroid reactions act as 'hubs' cap

39 Extreme pathway analysis showed progestin and corticosteroid synthesis reactions to be h

40 Estrogen plus progestin and estrogen alone decreased risk for fracture

41 the Women's Health Initiative Estrogen Plus Progestin and Estrogen-Alone Trials have been reported,

42 chorage-independent growth was stimulated by progestins and blocked by inhibition of Erk1/2, c-Src, E

43 rone, trans-androsterone, and testosterone), progestins and metabolites (progesterone, medroxyprogest

44 P4 transactivated the FHM nPR, whereas five progestins and P4 transactivated FHM AR, all at environm

45 ception", "HIV/acquisition", "injectables", "progestin", and "oral contraceptive pills".

46 33 steroids, including estrogens, androgens, progestins, and glucocorticoids, in hospital wastewaters

47 n of CK5(+) and CD44(+) cells in response to progestins, and results in increased stem-like propertie

48 t treatment of T47D breast cancer cells with progestin antagonized effects of fetal bovine serum (FBS

49 -based in vitro assays demonstrated that the progestins are all strongly androgenic, thereby explaini

50 Our discovery that progestins are capable of robust autocrine activation of

51 Progestins are components of human contraceptives and ho

52 Progestins are designed to activate human PR, but older

53 Synthetic progestins are widely used as a component in both contra

54 duction at very low concentrations makes the progestins arguably the most important pharmaceutical gr

55 ectable contraceptive that contains the same progestin as the menopausal hormone therapy regimen foun

56 ern that high-dose, long-lasting, injectable progestin-based contraception could mimic the high-proge

57 rpose of this study was to use estrogen- and progestin-based radiopharmaceuticals to image ERalpha an

58 High levels of progestin binding and progestin receptor (PR) mRNA have

59 st cancer models often remain insensitive to progestins, but are growth-inhibited by antiprogestins,

60 posthysterectomy women and of estrogen plus progestin by women with a uterus, along with correspondi

61 Barrier methods, intrauterine devices, and progestins can be used.

62 These progestins can bind to a wide range of receptors includi

63 ic progesterone used in contraception drugs (progestins) can promote breast cancer growth, but the me

64 ional data on estrogen and the estrogen plus progestin clinical trial and observational study data to

65 the effects of oestrogen alone or oestrogen-progestin combination therapy.

66 Women using estrogen plus progestin compared with placebo experienced significantl

67 .045) among women who received estrogen plus progestin compared with women in the placebo group.

68 Post-hoc analysis of the estrogen plus progestin component of the Women's Health Initiative stu

69 The possibility that progestins compromise ARV anti-HIV activity prompted us

70 n with intact uterus receiving estrogen plus progestin, considered separately, was not statistically

71 ks differed according to regimen and type of progestin constituent.

72 cused on combining antiretrovirals (ARV) and progestin contraceptives to prevent HIV infection and pr

73 nt use of various oral combination (estrogen-progestin) contraceptives varied between 1.0 and 1.6.

74 ontention that androgenic effects of certain progestins contribute to their reproductive toxicity.

75 r continuous use and no use of estrogen plus progestin crossed at about 6 years (CI, 2 years to 10 ye

76 cer associated with the use of estrogen plus progestin declined markedly soon after discontinuation o

77 t cancer models in which Stat3 is activated: progestin-dependent C4HD cells and 4T1 cells.

78 ents for their ability to prevent or inhibit progestin-dependent human breast tumors.

79 these regulatory regions were inhibited in a progestin-dependent manner following stimulation with pr

80 However, progestin-dependent progression of breast cancer tumor x

81 ounds that reactivate mutant p53 and prevent progestin-dependent progression of breast disease.

82 In this study, we used a murine progestin-dependent tumor to investigate the role of ERa

83 endothelial growth factor (VEGF); growth of progestin-dependent tumors is blocked by inhibiting synt

84 oral contraceptives (COCs) or the injectable progestins depot-medroxyprogesterone acetate (DMPA) or n

85 en together, the immunomodulatory effects of progestins differentially regulate the outcome of infect

86 The progestin drospirenone and P4 transactivated the FHM nPR

87 gs show potential for metformin and estrogen-progestin dual therapy but warrant longitudinal studies

88 ticularly for current users of estrogen plus progestin (E + P) menopausal hormone therapy (OR, 2.49;

89 rmone therapy with estrogen or estrogen with progestin (E + P) protected against cardiovascular disea

90 opposed estrogen (E-alone) and estrogen plus progestin (E+P) compared with placebo on a diverse set o

91 y was designed to test whether estrogen plus progestin (E+P) therapy favorably affects age-related ch

92 omen's Health Initiative (WHI) estrogen plus progestin (E+P) trial led to a substantial reduction in

93 ed with increasing duration of estrogen plus progestin (E+P) use (HR = 1.27 for E+P use 1 to 9 years,

94 women taking HRT, treated with estrogen and progestin (E+P; n = 32), estrogen alone (E; n = 30), and

95 Therefore, perhaps other approved progestins (e.g., NETA) should be considered as alternat

96 plus medroxyprogesterone acetate (2.5 mg/d [progestin]) (E + P) or placebo with a median interventio

97 Endogenous progestogens and pharmaceutical progestins enter the environment through wastewater trea

98 limited to women who had taken estrogen plus progestin (EP) preparations only (OR = 0.6, 95% CI 0.5-0

99 bind to a wide range of receptors including progestin, estrogen, androgen, glucocorticoid, and miner

100 with an H3N2 virus, female mice treated with progestins experienced greater mortality with increased

101 increased HIV acquisition in women with high progestin exposure.

102 aring women using only combined estrogen and progestin for 3 or more years with women using only unop

103 nds against the use of combined estrogen and progestin for the prevention of chronic conditions in po

104 nds against the use of combined estrogen and progestin for the primary prevention of chronic conditio

105 ind the best combination of testosterone and progestins for effective spermatogenesis suppression and

106 insulin-sensitizing agents, and (4) estrogen-progestin formulations.

107 A progestin further increased their already substantial pr

108 Progesterone (P4) and synthetic progestins (gestagens) from contraceptives and hormone t

109 Breast cancers in the estrogen-plus-progestin group were similar in histology and grade to b

110 en assigned to treatment with oestrogen plus progestin had a higher risk of cancer than did those ass

111 oderate certainty that combined estrogen and progestin has no net benefit for the primary prevention

112 The use of progestins has resulted in contamination of aquatic envi

113 ith combined HT supports the hypothesis that progestins have an attenuating effect on endometrial can

114 Seven of the progestins have been examined for their effects on aquat

115 ntamination of aquatic environments and some progestins have in experimental studies been shown to im

116 Progestins have long been used clinically for the treatm

117 ve of these (four synthetic and one natural) progestins have so far been studied in sewage effluent a

118 d to activate human PR, but older generation progestins have unwanted androgenic side effects in huma

119 that contained a combination of estrogen and progestin (hazard ratio, 1.37; 95% CI, 1.10-1.70) compar

120 us thromboembolism (VTE) may use estrogen or progestin hormonal therapy to control the menstrual blee

121 resulted from the mass cessation of estrogen-progestin hormone therapy (EPHT) in 2002.

122 Estrogen plus progestin hormone therapy (HT) is associated with an inc

123 trial cancer, whereas combined estrogen plus progestin hormone therapy is not.

124 of either estrogen alone or of estrogen plus progestin hormone therapy.

125 Among postmenopausal women, estrogen-progestin hormone use was predominantly associated with

126 .26), and, to a lesser extent, estrogen-plus-progestin HT (HR = 1.41, 95% CI: 1.08, 1.83), although r

127 sessed the association between estrogen plus progestin HT or unopposed estrogen HT and young-onset br

128 insertion of intrauterine devices (IUDs) or progestin implants and 20 to provide standard care.

129 Although treatment with oestrogen plus progestin in postmenopausal women did not increase incid

130 an equally potent and efficacious endogenous progestin in the horse but that the PR evolved with incr

131 endogenously synthesized DHP is a biopotent progestin in the horse ends decades of speculation, expl

132 initiated ET alone or in combination with a progestin in the late postmenopausal stage (ages 65-79 y

133 and reproductive effects of P4 and synthetic progestins in fish, and effects of the antiprogestin mif

134 score the need to evaluate neural actions of progestins in the rational design of hormone therapy.

135 se results reveal a novel mechanism, whereby progestins increase the stem cell-like population in hor

136 Estrogen plus progestin increased risk for breast cancer and probable

137 with normal cognition, estrogen and estrogen-progestin increased risk for dementia or a combined outc

138 Raloxifene, estrogen, and estrogen-progestin increased the risk for thromboembolic events,

139 Drospirenone (DRS) is a synthetic progestin increasingly used in oral contraceptives with

140 on on target gene promoters is essential for progestin-induced cell proliferation.

141 rential display) gene, first identified as a progestin-induced gene in T-47D breast cancer cells, enc

142 Progestin-induced rapid activation of cytoplasmic protei

143 Inhibition of JAK/STAT-signaling blocked progestin-induced STAT5A and Wnt1 expression.

144 tumor to investigate the role of ERalpha in progestin-induced tumor cell proliferation.

145 ollowing control for time from estrogen-plus-progestin initiation and confounding, hazard ratio estim

146 r recent sex) and being amenorrhoeic (due to progestin-injectable use), but not recent vaginal cleans

147 its association with recent vaginal sex and progestin-injectable use.

148 apy vary and the molecular mechanisms behind progestin insensitivity are poorly understood.

149 ment therapy (CHRT) containing estrogens and progestins is associated with breast cancer risk.

150 ument induction of the CK5-positive cells by progestins, it is unknown if other 3-ketosteroids share

151 teral displacement responses when endogenous progestin levels were elevated compared to when progesti

152 gestin levels were elevated compared to when progestin levels were lower.

153 But for the other synthetic progestins levels would need to reach tens or hundreds o

154 this study, the ability of the contraceptive progestin levonorgestrel to bind chemically with hydrosi

155 ations may result from the estrogen-like and progestin-like properties of chlordecone.

156 hyl-19-norpregna-4,9-dien-3,20-dione (R5020) progestin limited this effect and was counteracted by th

157 Progestin may enhance the estrogenic effect of conjugate

158 It has been suggested that progestins may have an inflammatory component and/or inc

159 eutic approach utilizing Akt inhibitors with progestins may improve the efficacy of progestin therapy

160 cent clinical trials indicate that synthetic progestins may stimulate progression of breast cancer in

161 ediated knockdown of endogenous PR abrogated progestin-mediated anti-proliferative effects.

162 /2, whereas siRNA knockdown of MKP-1 blocked progestin-mediated ERK1/2 dephosphorylation and repressi

163 dy, we investigated the role of microRNAs in progestin-mediated expansion of this dedifferentiated tu

164 Recombinant CCL2 reversed this progestin-mediated inhibition, whereas a STAT1 inhibitor

165 We found that treatment with the progestin medroxyprogesterone acetate (MPA) induced the

166 t both natural progesterone and the clinical progestin medroxyprogesterone acetate block estrogen neu

167 We also report that synthetic progestin medroxyprogesterone acetate promotes regressio

168 Women with a uterus received estrogen plus progestin (medroxyprogesterone acetate 2.5 mg/day) or pl

169 usal women, whereas combined estrogen plus a progestin (medroxyprogesterone acetate, MPA) HRT increas

170 urobiology of progesterone and the synthetic progestin, medroxyprogesterone acetate (MPA).

171 This study tests the progestin megestrol acetate (MA) at two doses versus pla

172 The role of the progestin megestrol acetate and, paradoxically, of tamox

173 cer model additionally included estrogen and progestin menopausal hormone therapy (MHT) use, other MH

174 The results strongly suggest that synthetic progestins merit serious consideration as environmental

175 evaluated interactions between CHRT use and progestin metabolism genotypes at CYP3A4 and the progest

176 be influenced by genetic factors involved in progestin metabolism.

177 e randomly assigned to receive estrogen plus progestin (n = 8,240), given as 0.625 mg/day conjugated

178 Sustained Erk1/2 activation in response to progestins occurred via a novel mechanism distinct from

179 The second experiment investigated two progestins of different potency: Gestodene at 1, 10, and

180 We aimed to assess the effects of progestins on HIV acquisition risk and the immune enviro

181 ivity prompted us to evaluate the effects of progestins on tenofovir (TFV) and TFV-alafenamide (TAF)

182 ne the potencies of four different synthetic progestins on the reproductive capabilities of the fathe

183 Weight gain, additional pregnancy, and progestin-only contraception are potential modifiable fa

184 betes, while additional pregnancy and use of progestin-only contraception were marginally associated

185 Injectable progestin-only contraceptive use and high endogenous pro

186 , including those associated with injectable progestin-only contraceptive use.

187 HIV-negative injectable progestin-only contraceptive users had 3.92 times the fr

188 l vasculature in women receiving long-acting progestin-only contraceptives (LAPCs) are unknown.

189 The use of injectable progestin-only contraceptives has been associated with i

190 Women using injectable progestin-only contraceptives were at substantially high

191 In this cohort, 152 women used injectable progestin-only contraceptives, 43 used other forms of co

192 similar immunological effects to injectable progestin-only contraceptives.

193 Of these eight, all reported findings for progestin-only injectables, and seven also reported find

194 Women who currently or recently used the progestin-only intrauterine system also had a higher ris

195 t of 1.8 (95% CI, 1.75-1.84) and those using progestin-only pills, 2.2 (95% CI, 1.99-2.52).

196 d products, 2.29 (95% CI=1.77-2.95) for oral progestin-only products, 2.58 (95% CI=2.06-3.22) for vag

197 ed for the on and off estrogen-containing or progestin-only therapy periods.

198 amic acid (during menstrual flow), high-dose progestin-only therapy, or combined hormonal contracepti

199 r, respectively, for estrogen-containing and progestin-only therapy.

200 persistent carriage among women and type of progestin or dose of estrogen used.

201 II trial of oral ridaforolimus compared with progestin or investigator choice chemotherapy (comparato

202 cation, (2) metformin vs placebo or estrogen-progestin oral contraceptives, (3) insulin-sensitizing a

203 mice were treated with placebo or one of two progestins, P4 or levonorgestrel (LNG), and infected wit

204 mean of 5.6 years among 16 128 estrogen plus progestin participants, and 683 cases over a mean of 7.1

205 the CK5-positive population by the synthetic progestin (Pg) R5020 in luminal breast cancer cells both

206 uited to the STC1 promoter in the absence of progestin; PR Lys-388 sumoylation was required for HDAC3

207 While the immunomodulatory properties of progestins protected immunologically naive female mice f

208 In FHMs, several progestins proved to be strong agonists of AR.

209 stosterone (T), alone or in combination with progestin, provides a promising approach to hormonal mal

210 ffects of progesterone (P4) or the synthetic progestin R5020 on ERK1/2 phosphorylation were independe

211 east cancer cells treated with the synthetic progestin R5020 revealed a subset of progesterone recept

212 inhibitor, MK-2206 (MK), in conjunction with progestin (R5020) treatment, is sufficient to upregulate

213 alpha), estrogen receptor-beta (ERbeta), and progestin receptor (PR) immunoreactivities are localized

214 or instance, the sex difference in perinatal progestin receptor (PR) immunoreactivity in the medial p

215 High levels of progestin binding and progestin receptor (PR) mRNA have also been reported in

216 of estrogen receptor (ER) alpha, ERbeta and progestin receptor (PR) with LENK-labeled MF pathway pro

217 ptic connectivity maybe mediated through the progestin receptor (PR).

218 -1 down-regulated the expression of membrane progestin receptor alpha (mPRalpha), the intermediary in

219 post-synaptic GPCRs, including the membrane progestin receptor, the corticotropin releasing hormone

220 However, the distribution of progestin receptors (PR) in a socially monogamous and sp

221 Progesterone and progestin receptors (PRs) are known to play a role in th

222 ve no detectible impact on the expression of progestin receptors.

223 e (WHI) clinical trial, use of estrogen plus progestin reduced the colorectal cancer diagnosis rate,

224 Progestins reduced the antibody responses during primary

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

226 phorylation of PR Ser81 is ck2 dependent and progestin regulated in intact cells but also occurs in t

227 ed Ser79/81 phosphorylation for basal and/or progestin-regulated (BIRC3, HSD11beta2, and HbEGF) expre

228 alth Initiative (WHI) and Heart and Estrogen/Progestin Replacement Study (HERS), studied the role of

229 e genotyped 2090 women in Heart and Estrogen/progestin Replacement Study for functional polymorphisms

230 tional activity, leading to overall impaired progestin responses.

231 Estrogen plus progestin results among women who initiated use soon aft

232 We show that the contraction-associated and progestin-sensitive genes (oxytocin receptor, connexin 4

233 This study suggests that progestins significantly affect adaptive immune response

234 assays performed in the absence of exogenous progestin; similar results were obtained in PR-null/ER+

235 iodine-substituted 16alpha,17alpha-dioxolane progestins, some of which, when appropriately radiolabel

236 (p=0.0488), suggesting that a naturally high progestin state had similar immunological effects to inj

237 The antiprogestin RU-486 blocks progestin stimulation of growth, indicating involvement

238 re increased for estrogen (stroke), estrogen-progestin (stroke, coronary heart disease, invasive brea

239 Prior progestin studies treating hot flashes in women have bee

240 Some progestins, such as levonorgestrel (LNG), exert androgen

241 tive (WHI) indicated that long-term estrogen/progestin supplementation led to increased incidence of

242 ysis of cofactor usage (O2 and NADPH) showed progestin synthesis reactions to exhibit high robustness

243 agnoses in the group receiving estrogen plus progestin than in the placebo group in the initial 2 yea

244 ulations, including those that contain newer progestins that lower blood pressure, as well as the non

245 alth Initiative (WHI) trial of estrogen plus progestin, the use of menopausal hormone therapy in the

246 suggest a potential target of environmental progestins, the circadian rhythm network, in addition to

247 3.93, 95% CI: 1.43, 10.84), or estrogen-plus-progestin therapy (OR = 3.51, 95% CI: 1.45, 8.49).

248 with progestins may improve the efficacy of progestin therapy for the treatment of endometrial cance

249 Estrogen plus progestin therapy increases the risk for coronary heart

250 It showed that estrogen plus progestin therapy reduced fractures (46 fewer per 10 000

251 rial cancers; however, the response rates to progestin therapy vary and the molecular mechanisms behi

252 rd ratio for continuous use of estrogen plus progestin therapy was 2.36 (95% CI, 1.55 to 3.62) for th

253 Use of estrogen-plus-progestin therapy was not associated with the risk of pa

254 endometrioid tumors were found with estrogen/progestin therapy, whereas no association was found with

255 Addition of progestins to androgens improved the rate of suppression

256 ted recent inconsistent findings that adding progestins to postmenopausal estrogen replacement therap

257 s, this study confirms the benefit of adding progestins to the regimen.

258 or (pdC1-INH) for acute swelling attacks and progestins, tranexamic acid, and danazol for the prevent

259 ion of prolactin, a decidual marker gene, in progestin-treated HESCs without the need of simultaneous

260 glutinin stalk antibody titers were lower in progestin-treated mice than placebo-treated mice.

261 ters were relatively decreased in estrogen + progestin-treated tumors.

262 hich this occurs, we documented that chronic progestin treatment blunted ER-mediated gene expression

263 In contrast to primary IAV infection, progestin treatment increased the titers of neutralizing

264 Progestin treatment of T47D cells rapidly induced MKP-1

265 n contrast, following challenge with maH3N2, progestin treatment reduced survival as well as the numb

266 1 PR-B was recruited to the STAT5A gene upon progestin treatment, suggestive of a feed-forward mechan

267 2 years) and 2679 women in the estrogen-plus-progestin trial (aged 63-87, mean 72 years).

268 -1.24; P=0.05), but not in the estrogen plus progestin trial (hazard ratio, 1.07; CI, 0.91-1.25; P=0.

269 led from 1993 to 1998, and the estrogen plus progestin trial was stopped on July 7, 2002.

270 In the estrogen-plus-progestin trial, there was no association for total arth

271 In the estrogen-plus-progestin trial, there was no significant difference in

272 from the Women's Health Initiative estrogen-progestin trial, which found that menopausal hormone the

273 he corresponding relative risks according to progestin type were as follows: desogestrel, 1.5 (1.3 to

274 ively small differences in risk according to progestin type.

275 roke and myocardial infarction, according to progestin type: norethindrone, 2.2 (1.5 to 3.2) and 2.3

276 Progestins, UPR activation and perhaps reduced ICI-stimu

277 PR/progestin upregulated epidermal growth factor receptor (

278 ger association in postmenopausal women with progestin use (beta=-0.028, p=7.3x10(-5)) than in those

279 tified gene-environment interactions between progestin use and MUC1 and between insulin and TRPM6 on

280 Thus, extended progestin use may be associated with higher risk of peri

281 h baseline aspirin use and combined estrogen-progestin use status (P = .01 for each).

282 e use, bilateral oophorectomy, estrogen plus progestin use, and height.

283 easing time from initiation of estrogen-plus-progestin use, and observational study hazard ratio esti

284 These findings differ from estrogen-plus-progestin use, for which significantly increased abnorma

285 nd within the first 2 years of estrogen plus progestin use, including in women who initiated therapy

286 Norethindrone acetate (NETA), another progestin used in HRT, acts like an estrogen at high dos

287 to medroxyprogesterone acetate, a synthetic progestin used in postmenopausal hormone replacement the

288 ow-up, 289 estradiol users and 196 estradiol-progestin users were diagnosed with meningioma.

289 31,480 estradiol users and 131,248 estradiol-progestin users), and meningioma cases were identified f

290 0.7% to 1.1%) for estrogen and estrogen plus progestin users.

291 .2% (95% CI, 3.7% to 4.6%) for estrogen plus progestin users.

292 nsity (BIRADS-4), particularly estrogen plus progestin users: women age 55 to 59 years, 5-year risk w

293 alth Initiative (WHI) trial of estrogen plus progestin vs placebo was stopped early, after a mean 5.6

294 Estrogen plus progestin was associated with greater breast cancer inci

295 l follow-up on March 31, 2005, estrogen plus progestin was associated with more invasive breast cance

296 Use of estrogen plus progestin was not associated with an increased risk of y

297 riptional activity occurred independently of progestins, was increased by activated CDK2, and attenua

298 ast cancer, where both natural and synthetic progestins were found to antagonize the mitogenic effect

299 in the presence or absence of estradiol and progestin, whereas LMMP readily grew under these conditi

300 (MPA) and dydrogesterone (DDG) are synthetic progestins widely used in human and veterinary medicine.

301 an oral contraceptive in combination with a progestin, without increasing the level of coagulation f