ライフサイエンスコーパス: endometrial

1 ndometrial cancer (49%); PIK3CA mutations in endometrial (37%), breast (31%), cervical (29%), and ana

2 tumors are hypothesized to develop from the endometrial adenocarcinoma (EAC) through epithelial-mese

3 al kisspeptin signaling is indispensable for endometrial adenogenesis and function, essential aspects

4 alpha (ERalpha) is highly expressed in both endometrial and breast cancers, and represents the most

5 diated degradation of the ERalpha protein in endometrial and breast cells.

6 However, the molecular mechanism underlying endometrial and breast safety during TSEC use is not ful

7 Therefore, the endometrial and breast safety effects of TSEC are associ

8 s been shown to contribute to oncogenesis in endometrial and cervical carcinomas.

9 yroid and testicular cancers to >10/tumor in endometrial and colorectal cancers.

10 Human endometrial and mouse uterine cytokine/chemokine mRNA co

11 A significant proportion of colon, endometrial and ovarian cancers exhibit k-h expression/c

12 , including in dose-response associations in endometrial and post-menopausal breast cancer, and in de

13 main of the ubiquitin ligase adaptor SPOP in endometrial and prostate cancers.

14 ography is an imaging method to evaluate the endometrial and uterine morphology and fallopian tube pa

15 a diagnostic phenotype for gastrointestinal, endometrial, and colorectal tumors, yet the landscape of

16 Findings from these trials in breast, endometrial, and ovarian cancer are reviewed.

17 decreased risk of breast, colorectal, colon, endometrial, and prostate cancers; cardiovascular diseas

18 s with Lynch syndrome-associated colorectal, endometrial, and/or ovarian cancers whose medical record

19 Intracrine biosynthesis of endometrial androgens during decidualization may play a

20 n samples revealed time-dependent changes in endometrial apoptosis preceding neutrophil influx and cy

21 ne expression profiles from mid-luteal phase endometrial biopsies (n = 115) from women experiencing R

22 tween DNA methylation and gene expression in endometrial biopsies collected from 17 healthy fertile-a

23 Endometrial biopsies were taken and total RNA extraction

24 use of BET inhibitors to treat patients with endometrial but not prostate cancer who harbor SPOP muta

25 nt between-group difference in recurrence of endometrial cancer (28/353 in TAH group [7.9%] vs 33/407

26 al (48%), gastric (36%), prostate (52%), and endometrial cancer (49%); PIK3CA mutations in endometria

27 Endometrial cancer (EC) remains the most common malignan

28 ismatch repair (MMR) defects in endometrioid endometrial cancer (EEC) has not been definitively estab

29 al integrity and suggest why loss of CD73 in endometrial cancer allows for tumor progression.

30 adiposity was an independent risk factor for endometrial cancer among black women and appeared to exp

31 s meta-analysis suggest an increased risk of endometrial cancer among patients with hypertension, how

32 egulation of uterine cell growth can lead to endometrial cancer and infertility.

33 sk of oral, pharynx, liver, colon, prostate, endometrial cancer and melanoma and increased lung cance

34 on oral, pharyngeal, colon, liver, prostate, endometrial cancer and melanoma, with RR 0.69 (95% CI =

35 Seventy percent of patients with endometrial cancer and more than 50% of patients with br

36 Secondary outcomes included recurrence of endometrial cancer and overall survival.

37 detecting distant metastasis in cervical and endometrial cancer and should be included in the staging

38 sk estimates and 95% confidence intervals of endometrial cancer associated with a hypertension diagno

39 ation carriers presented with colorectal and endometrial cancer at later ages than carriers of mutati

40 Seven patients were diagnosed with endometrial cancer based on classic histopathologic anal

41 he comprehensive, genomics-based analysis of endometrial cancer by The Cancer Genome Atlas (TCGA) rev

42 WAS) and two follow-up phases totaling 7,737 endometrial cancer cases and 37,144 controls of European

43 ing genotyped and imputed SNP data for 6,608 endometrial cancer cases and 37,925 controls of European

44 ian cancer cases with 1,356 controls and 532 endometrial cancer cases with 1,286 controls.

45 factorial ChIP-seq data integration from the endometrial cancer cell line Ishikawa illustrated a func

46 activity were investigated using ovarian and endometrial cancer cell lines.

47 ere we find that PTEN-deficient endometrioid endometrial cancer cells are not responsive to PARP inhi

48 ERalpha was found at active enhancers in endometrial cancer cells as marked by the presence of RN

49 rendered PTEN wild-type Hec-1A endometrioid endometrial cancer cells responsive to combined inhibiti

50 hereditary CRC and population-based CRC and endometrial cancer cohorts, possibly biasing results.

51 cancer types, the incidence and mortality of endometrial cancer continue to grow.

52 s with cervical cancer and 203 patients with endometrial cancer enrolled at 28 sites.

53 the Black Women's Health Study for incident endometrial cancer from 1995 through 2013 (n = 274).

54 We conducted a meta-analysis of three endometrial cancer genome-wide association studies (GWAS

55 About 15% of patients with endometrial cancer have high-risk features and are at in

56 al cancer in 249 (61%) of 409 men and women; endometrial cancer in 53 of 196 (27%) women; and ovarian

57 nly associated with female-specific cancers: endometrial cancer in 83 (30%) of 279 women; ovarian can

58 t extent these factors influence the risk of endometrial cancer in black women.

59 n of breast cancer, it increases the risk of endometrial cancer in postmenopausal women.

60 n has been associated with increased risk of endometrial cancer in several studies, but the results h

61 l-regionally advanced cervical and high-risk endometrial cancer in the clinical trial by the American

62 s among weight change by intentionality with endometrial cancer in the Women's Health Initiative (WHI

63 , have been associated with a higher risk of endometrial cancer in white women.

64 [HRs] and 95% CIs) between weight change and endometrial cancer incidence.

65 Standard treatment for endometrial cancer involves removal of the uterus, tubes

66 fter radiotherapy in patients with high-risk endometrial cancer is feasible, with rapid recovery afte

67 As therapy against cancer stem cells in endometrial cancer is lacking, the ability of anti-EMP2

68 The association between LOC and endometrial cancer is less certain.

69 Endometrial cancer is the most common gynaecological tum

70 Endometrial cancer is the most common gynecologic cancer

71 Endometrial cancer is the most common gynecologic malign

72 Endometrial cancer is the most common gynecological mali

73 Endometrial cancer is the most common malignancy of the

74 to high risks of colorectal cancer (CRC) and endometrial cancer mainly as a result of mutations in ML

75 h degree of diagnostic accuracy in detecting endometrial cancer metastases and can safely replace lym

76 and PPV of PET/CT detection of cervical and endometrial cancer metastases were all significantly hig

77 11.4 years (mean) of follow-up, 566 incident endometrial cancer occurrences were confirmed by medical

78 cohort study patients with clinical stage 1 endometrial cancer of all histologies and grades undergo

79 the interval time between breast cancer and endometrial cancer only in tamoxifen-treated breast canc

80 enhance the activity of megestrol acetate in endometrial cancer patients, we explored the potential o

81 gestrol acetate is a frequently used drug in endometrial cancer patients.

82 ly and disease recurrence postoperatively in endometrial cancer patients.

83 l role of mutation of PPP2R1A in ovarian and endometrial cancer progression remains unclear.

84 ell carcinomas and has some association with endometrial cancer relapse and metastasis.

85 n with weight loss had a significantly lower endometrial cancer risk (HR, 0.71; 95% CI, 0.54 to 0.95)

86 Identification of an endometrial cancer risk allele within a member of the PI

87 and OR = 2.44 (95% CI: 1.22, 4.87)) and with endometrial cancer risk as computed by 1 algorithm (OR =

88 Purpose Although obesity is an established endometrial cancer risk factor, information about the in

89 ns of dietary LC omega-3 PUFAs and fish with endometrial cancer risk in 47,602 African-American women

90 mation about the influence of weight loss on endometrial cancer risk in postmenopausal women is limit

91 (>/= 10 pounds) was associated with a higher endometrial cancer risk than was stable weight, especial

92 tmenopausal women is associated with a lower endometrial cancer risk, especially among women with obe

93 (quintiled) and fish (quartiled) intake with endometrial cancer risk, overall and by body mass index

94 stimulatory effects of rs2494737 increasing endometrial cancer risk.

95 ify the association between hypertension and endometrial cancer risk.

96 ted the associations of LOC with ovarian and endometrial cancer risks using unconditional logistic re

97 P2 therapy may be a novel method of reducing endometrial cancer stem cells.

98 he rs9600103[T] allele that is protective in endometrial cancer suppressed gene expression in vitro,

99 e with truncating MLH1 mutations could begin endometrial cancer surveillance later than those with no

100 ng MLH1 mutations had later ages of onset of endometrial cancer than those with nontruncating mutatio

101 ion of gene methylation are recapitulated in endometrial cancer tissue samples obtained from patients

102 ndomized 760 women with stage I endometrioid endometrial cancer to either TLH or TAH.

103 ne (P4) has been used for several decades in endometrial cancer treatment, especially in women who wi

104 The association between hypertension and endometrial cancer was weaker, but still significant, am

105 ncer and 121 700 (38.4%) of 317 000 cases of endometrial cancer were attributable to these risk facto

106 s were noted, and the risk of colorectal and endometrial cancer were markedly increased in first-, se

107 Women with high-risk endometrial cancer were randomly allocated (1:1) to radi

108 Here, we identified a patient with endometrial cancer who had an exceptional response to th

109 In 8 patients (with either ovarian or endometrial cancer), after a staging lymphadenectomy inc

110 st cancer, one in ovarian cancer, and one in endometrial cancer).

111 women with colorectal cancer, 162 women with endometrial cancer, and 49 women with ovarian cancer; me

112 For postmenopausal breast and endometrial cancer, every 10-y increase in adulthood ove

113 l between breast cancer and the emergence of endometrial cancer, exclusively in tamoxifen-treated pat

114 aclitaxel (PTX), the frontline treatment for endometrial cancer, in tumours with mutant p53 and enhan

115 rcinoma, one of the most aggressive types of endometrial cancer, is characterized by poor outcomes an

116 is versus 64.6%, 98.6%, 86.1%, and 95.4% for endometrial cancer, respectively.

117 tasis and 66.7%, 93.9%, 59.3%, and 95.5% for endometrial cancer, respectively.

118 ) values were 0.78 and 0.89 for cervical and endometrial cancer, respectively; these were not signifi

119 Among women with stage I endometrial cancer, the use of total abdominal hysterect

120 In a xenograft model of endometrial cancer, this combinatorial therapy resulted

121 ne-binding alterations of ERalpha in primary endometrial cancer, with potentially important therapeut

122 bstrates that are preferentially degraded by endometrial cancer-associated SPOP mutants.

123 hanges in the ubiquitin landscape induced by endometrial cancer-associated SPOP mutations and identif

124 at increased risk of distant metastases and endometrial cancer-related death.

125 ce is essential to improve the therapies for endometrial cancer.

126 polarity) for genetic alterations of CTCF in endometrial cancer.

127 ly replace lymphadenectomy in the staging of endometrial cancer.

128 erectomy (TAH) in women with treatment-naive endometrial cancer.

129 enectomy in detecting metastatic disease for endometrial cancer.

130 roscopic hysterectomy for women with stage I endometrial cancer.

131 t common genetic aberrations in endometrioid endometrial cancer.

132 ts in individuals at high risk of developing endometrial cancer.

133 d to treat breast cancer, increases risks of endometrial cancer.

134 subunit alpha gene (PIK3CA) are frequent in endometrial cancer.

135 ective screening methodology or protocol for endometrial cancer.

136 processes and the pathogenesis of breast and endometrial cancer.

137 herapy has not been shown to be effective in endometrial cancer.

138 on of interest for genetic susceptibility to endometrial cancer.

139 in the Pten(d/d) conditional mouse model of endometrial cancer.

140 erties of cells that promote EMT in advanced endometrial cancer.

141 r screening women for the earliest stages of endometrial cancer.

142 ose tissue contribute to the pathogenesis of endometrial cancer.

143 he risk of developing cancer, especially for endometrial cancer.

144 ha in breast cancer and tamoxifen-associated endometrial cancer.

145 compromise long-term survival for women with endometrial cancer.

146 ined from patients with tamoxifen-associated endometrial cancer.

147 c mouse model of Pten-deficient endometrioid endometrial cancer.

148 ance in human reproductive diseases, such as endometrial cancer.

149 ated as an alternative staging technique for endometrial cancer.

150 signing PIK3 pathway targeting strategies in endometrial cancer.

151 or cervical cancer and 11.8% (24 of 203) for endometrial cancer.

152 CTCF is frequently mutated in endometrial cancer.

153 rol acetate combination for the treatment of endometrial cancer.

154 tion associated with increased expression in endometrial cancer.

155 tion of abdominal LN metastasis in high-risk endometrial cancer.

156 ting lymph node (LN) metastasis in high-risk endometrial cancer.

157 Endometrial cancers (ECs) are one of the most common typ

158 ected in all 13 patients with double somatic endometrial cancers (P = .04 compared with other subgrou

159 monstrate extensive genetic heterogeneity in endometrial cancers and relative homogeneity across meta

160 More than half of endometrial cancers are currently attributable to obesit

161 ore than 30% of bladder, colon, gastric, and endometrial cancers have NsM counts above 192, which was

162 e utility of PARP inhibitors to endometrioid endometrial cancers in a PTEN-deficient setting.

163 roductive pathologies, including ovarian and endometrial cancers in the female reproductive tract.

164 ween puberty timing and risks for breast and endometrial cancers in women and prostate cancer in men.

165 ed exon9 and exon20 of PIK3CA in 280 primary endometrial cancers to assess the relationship with clin

166 lnerabilities of PTEN-deficient endometrioid endometrial cancers to PARP inhibition remain controvers

167 Risks of colorectal and endometrial cancers were also found to be elevated in se

168 mpared ERalpha sites in tamoxifen-associated endometrial cancers with publicly available ERalpha ChIP

169 g colorectal cancer (and advanced adenomas), endometrial cancers, and breast cancer.

170 ve detailed the genomic landscape of primary endometrial cancers, but the evolution of these cancers

171 We hypothesized that in PTEN-mutated endometrial cancers, hyperactive Akt signaling downregul

172 nt tumors represent only a small fraction of endometrial cancers, the therapeutic utility of PARP inh

173 ble for patients with advanced and recurring endometrial cancers.

174 ng been used clinically for the treatment of endometrial cancers; however, the response rates to prog

175 ggest that ADAR2 functions as an oncogene in endometrial carcinogenesis and could be a potential targ

176 alterations that occur frequently in serous endometrial carcinoma (EC) and carcinosarcoma, two clini

177 to MYC in lung adenocarcinoma (MYC-LASE) and endometrial carcinoma (MYC-ECSE) are physically associat

178 increased in vitro migration and invasion of endometrial carcinoma cells.

179 in poorly differentiated and advanced-stage endometrial carcinoma compared with levels in normal end

180 ypothesized that CD73-generated adenosine in endometrial carcinoma induces an innate reflex to protec

181 No increased risk for endometrioid endometrial carcinoma or sarcoma was found after stratif

182 al membrane protein-2 (EMP2) correlates with endometrial carcinoma progression and ultimately poor su

183 t increased, the risk for serous/serous-like endometrial carcinoma was increased in BRCA1+ women.

184 l carcinoma, melanoma, thyroid carcinoma and endometrial carcinoma).

185 th THSD7A-associated MN and metastases of an endometrial carcinoma, immunohistochemistry showed THSD7

186 current lesion in uterine carcinosarcoma and endometrial carcinoma.

187 urrent Rheb Tyr35Asn mutations in kidney and endometrial carcinoma.

188 urrence in women with early-stage, low-grade endometrial carcinoma.

189 n women with presumed early-stage, low-grade endometrial carcinoma?

190 Cancer Genome Atlas (TCGA), we observe that endometrial carcinomas manifest recurrent ESR1 gene ampl

191 rous and/or serous-like (serous/serous-like) endometrial carcinomas were observed (4 BRCA1+ and 1 BRC

192 serous cystadenocarcinoma and uterine corpus endometrial carcinomas.

193 Here we characterise the endometrial CD8-T cell population during the embryonic w

194 ic bacteria and LPS were modulated in bovine endometrial cell and organ cultures by small molecules t

195 Glycosylation of uterine endometrial cells plays important roles to determine the

196 h IGF-1R/PI3K/Akt signaling pathway in human endometrial cells.

197 and geranylgeranyl diphosphate, also reduced endometrial cellular inflammatory responses to LPS.

198 oinsufficiency also occurs in poor prognosis endometrial clear cell carcinomas and has some associati

199 ree mutations in MSH6 and PMS2 that increase endometrial, colorectal, brain and ovarian cancer risk.

200 , two patients had ovarian simple cysts, two endometrial cysts, three dermoid cysts, one patient had

201 IL-4(-/-) and IL-4Ralpha(-/-) mice displayed endometrial damage not seen in wild-type or IL-10(-/-) m

202 proliferation and prevent Chlamydia-induced endometrial damage.

203 ily 1 member C3/AKR1C3), b) establishment of endometrial decidualization (IGFBP1, prolactin) and c) e

204 t that miR-542-3p plays an important role in endometrial decidualization by regulating the expression

205 Endometrial decidualization represents an essential step

206 s in sexual behavior, ovulation, and uterine endometrial differentiation.

207 Using our targeted sequencing approach, endometrial driver mutations were identified in all seve

208 ine models, CD73 deficiency led to a loss of endometrial epithelial barrier function, and pharmacolog

209 we developed a human three-dimensional (3-D) endometrial epithelial cell (EEC) model using the HEC-1A

210 ory targets of TTP in both endometriotic and endometrial epithelial cell lines.

211 Here we show that both human and murine endometrial epithelial cells express the high affinity N

212 Silencing of TTP in endometriotic and endometrial epithelial cells revealed differential respo

213 scription 3 (STAT3) and proliferation of the endometrial epithelial cells.

214 nctional/structural characteristics of human endometrial epithelial tissue, including cell differenti

215 In vitro stimulation of endometrial epithelial, endothelial and endometriotic ep

216 women with recurrent miscarriage have lower endometrial expression of FST during the luteal phase.

217 who received placebo; there were no adverse endometrial findings.

218 bacteria were present in focal areas between endometrial folds (6/6 mares).

219 the involvement of exosomes in mid-secretory endometrial functions.

220 Uterine growth and endometrial gland formation (adenogenesis) and function,

221 CF in the regulation of cellular polarity of endometrial glandular epithelium.

222 Endometrial glycogen content, litter size and weight of

223 d throughout early pregnancy, is the rise in endometrial glycogen content.

224 veal a novel mechanism establishing adequate endometrial glycogen stores for pregnancy.

225 to female reproductive disorders, including endometrial hyperplasia and breast cancer.

226 Female mutant mice develop endometrial hyperplasia due to aberrant phosphorylation

227 ce of a differing pre-pregnancy phenotype in endometrial immune cells in RM.

228 ly cervical infection to those in women with endometrial infection and frequencies in women who remai

229 66 [95% CI, 1.07-2.60]) were associated with endometrial infection.

230 icovaginal fluid from women with symptoms of endometrial lesions, women appearing in the clinic for a

231 wed eosinophils were the main IL-4-producing endometrial leukocyte (constitutively and during Chlamyd

232 amination, mammogram, uterine ultrasound, or endometrial lining biopsy.

233 st fibrocystic disease, uterine fibroids, or endometrial lining thickness as assessed by clinical exa

234 ssociated with decreased risk of colorectal, endometrial, lung, and pancreatic cancers.

235 normal cells such as dermal fibroblasts and endometrial mesenchymal stem cells.

236 rofile, although not much is known about the endometrial methylome changes throughout the menstrual c

237 damental to the establishment of a receptive endometrial microenvironment which can support and maint

238 The endometrial mucosa is populated by a variety of immune c

239 2, HER2) in diverse human tumours (prostate, endometrial, ovarian and gastric), using various tissue

240 s that predispose individuals to colorectal, endometrial, ovarian, and other cancers through inactiva

241 ntly differ from that of controls in breast, endometrial, pancreas, or colorectal adenocarcinomas.

242 l decidualization (IGFBP1, prolactin) and c) endometrial receptivity (SPP1, MAOA, EDNRB) were measure

243 uring decidualization may play a key role in endometrial receptivity and offer a novel target for fer

244 We identify a meta-signature of endometrial receptivity involving 57 mRNA genes as putat

245 and prolactin and altered the expression of endometrial receptivity markers.

246 as promising and sought-after biomarkers of endometrial receptivity, fertility and infertility.

247 nd down-regulated genes that are involved in endometrial receptivity.

248 Here we perform a meta-analysis of endometrial-receptivity associated genes on 164 endometr

249 ntifies 348 microRNAs that could regulate 30 endometrial-receptivity associated genes, and we confirm

250 ur understanding of the role of androgens in endometrial repair and suggest that androgens may have d

251 ied this innate immune cell as essential for endometrial repair during Chlamydia infection.

252 Endometrial repair is normally both rapid and scarless.

253 e cutaneous wound healing, but their role in endometrial repair is unknown.

254 to treat conditions associated with aberrant endometrial repair processes.

255 ion levels in extraembryonic tissues and the endometrial response to altered signaling from clones.

256 ometrial-receptivity associated genes on 164 endometrial samples (76 from 'pre-receptive' and 88 from

257 Several HKGs not previously tested in endometrial samples were found to be more stable than th

258 6/6 mares and 5/6 mares, respectively, from endometrial samples with tissue-adherent bacteria (P < 0

259 P2R1A has been observed at high frequency in endometrial serous carcinomas but at low frequency in ov

260 Endometrial SLC5A1 expression during the implantation wi

261 antitumor effects of P4 are mediated by the endometrial stroma.

262 Successful implantation requires endometrial stromal cell (ESC) decidualisation.

263 ha and STAT6 signaling mediated IL-4-induced endometrial stromal cell (ESC) proliferation ex vivo, an

264 e expression of GPR64 was increased in human endometrial stromal cells (hESCs) during in vitro decidu

265 ulation of decidual gene expression in human endometrial stromal cells (HESCs).

266 ng is crucial for the decidualization of the endometrial stromal cells for successful pregnancy.

267 We isolated human endometrial stromal cells from nonpregnant donors with a

268 tal placental trophoblast cells and maternal endometrial stromal cells, using single-cell transcripto

269 has a crucial role in the decidualization of endometrial stromal cells.

270 upregulated upon decidualization of primary endometrial stromal cells.

271 lls differentiate from their precursors, the endometrial stromal fibroblasts, during uterine preparat

272 Following infection, the endometrial surface contained focal areas of bacterial g

273 nfection, the horses were euthanized and the endometrial surfaces were imaged for luminescence to loc

274 The eQTL for LINC00339 was also observed in endometrial tissue (P = 2.4 x10-8) with the same directi

275 ed from whole blood from 862 individuals and endometrial tissue from 136 individuals from independent

276 st that androgens may have direct impacts on endometrial tissue integrity.

277 hat is categorized by the abnormal growth of endometrial tissue outside the uterus.

278 idomic profile of 39 human EC and 17 healthy endometrial tissue samples.

279 s on which HKGs are most stably expressed in endometrial tissue so this study aimed to identify the m

280 direction of effect for both whole blood and endometrial tissue.

281 Well-characterised endometrial tissues from women were compared with uteri

282 Functional analysis of DEGs in placental and endometrial tissues suggests a major disruption of signa

283 the aforementioned HKG for normalisation of endometrial tissues taken from patients with RM and RIF.

284 ch of fertilized oocytes, and found ratio of endometrial to myometrial thicknesses in abdominal ultra

285 Immunohistochemical analysis of 230 primary endometrial tumor specimens showed that lack of FOXA1 an

286 Ralpha-binding sites in tamoxifen-associated endometrial tumors differed from those in the tumors fro

287 umors from tamoxifen users with those of six endometrial tumors from nonusers and integrated these re

288 dometrial tumors from tamoxifen users and 64 endometrial tumors from nonusers.

289 e results with the transcriptomic data of 47 endometrial tumors from tamoxifen users and 64 endometri

290 seq), we compared the ERalpha profiles of 10 endometrial tumors from tamoxifen users with those of si

291 ERalpha transcriptional action in breast and endometrial tumors have been found that might explain th

292 Our study highlights the divergence between endometrial tumors that arise in different hormonal cond

293 binding signature of ERalpha differs between endometrial tumors that arise in the presence or absence

294 , we identified patients with colorectal and endometrial tumors who had 2 or more somatic (but not ge

295 Some colorectal and endometrial tumors with microsatellite instability not a

296 as (113 patients with colorectal tumors, 178 endometrial tumors); 100% of double somatic cases had a

297 intracellular signaling pathway activated in endometrial tumors.

298 e been found in many sporadic colorectal and endometrial tumors.

299 prostate, 7; breast, 5; pancreas, 5; ovarian/endometrial/vulvar cancers, 3; and de novo cholangiocarc

300 Androgens regulate scarless repair of the endometrial "wound" in a mouse model of menstruation.