ライフサイエンスコーパス: endometrial

1 ous pelvic cancers (11 cervical, 2 rectal, 1 endometrial).

2 er risk in men), breast (6%-10% lower risk), endometrial (10%-18% lower risk), kidney (11%-17% lower

3 ble MMAS score of 100 than women assigned to endometrial ablation (180 [69%] of 262 women vs 146 [54%

4 Endometrial ablation aims to treat heavy menstrual bleed

5 h their operation compared with those in the endometrial ablation group (270 [97%] of 278 women vs 24

6 ectomy group and 11 (4%) of 307 women in the endometrial ablation group had at least one serious adve

7 ic supracervical hysterectomy is superior to endometrial ablation in terms of clinical effectiveness

8 laparoscopic supracervical hysterectomy with endometrial ablation in women seeking surgical treatment

9 menstrual bleeding and who were eligible for endometrial ablation were randomly allocated (1:1) to ei

10 is effective but has more complications than endometrial ablation, which is less invasive but ultimat

11 racervical hysterectomy or second generation endometrial ablation.

12 he most common histologies were endometrioid endometrial adenocarcinoma (n = 13), prostate adenocarci

13 Endometrial adenocarcinoma arises from the uncontrolled

14 rone receptor cre ("Alk5 cKO") that develops endometrial adenocarcinoma with metastasis to the lungs.

15 nism for hormone-independent pathogenesis of endometrial adenocarcinoma.

16 NA genesis, also plays a significant role in endometrial adenocarcinoma.

17 ineered mouse model of poorly differentiated endometrial adenocarcinoma.

18 en in mice resulted in poorly differentiated endometrial adenocarcinomas, which expressed Napsin A an

19 are significantly altered by the presence of endometrial and breast cancer.

20 Furthermore, TAMs from endometrial and breast cancers are transcriptionally dis

21 We collected endometrial and cervical biopsies from women using the l

22 ntraceptives of by studying their effects on endometrial and cervical transcriptomes.

23 pair (MMR), occurs frequently in colorectal, endometrial and gastric cancers.

24 s represent healthier behavior) with risk of endometrial and ovarian cancers among 108,136 postmenopa

25 Lifestyle-related factors influence risk of endometrial and ovarian cancers, but few studies have ex

26 naecological malignancies, such as cervical, endometrial and ovarian cancers, through direct and indi

27 ck, lung, breast, gastrointestinal, ovarian, endometrial and prostate cancer, mesothelioma, melanoma,

28 omatic variants in SPOP are cancer specific; endometrial and prostate cancers result from gain-of-fun

29 We find that bovine endometrial and skin fibroblasts are more resistant to i

30 Previous work has linked endometrial ARID1A loss to endometriosis-related endomet

31 isation in quantitative RT-PCR studies using endometrial biopsies obtained from women with endometria

32 pithelial organoid (EEO) cultures from human endometrial biopsies.

33 Incidence rates for endometrial cancer (EC) are rising, particularly in post

34 of patients with colorectal cancer (CRC) and endometrial cancer (EC) to better determine the utility

35 formed in patients with colorectal (CRC) and endometrial cancer (EC) to screen for Lynch syndrome (LS

36 (LS)-associated colorectal cancer (CRC) and endometrial cancer (EC), but they have not been assessed

37 Lynch syndrome (LS) predisposes to endometrial cancer (EC), colorectal cancer, and other ca

38 otherapy alone (RT) for women with high-risk endometrial cancer (EC).

39 atch repair-proficient (MMRP) and -deficient endometrial cancer (EC).

40 Endometrial cancer (EMCA) is a clinically heterogeneous

41 best reference genes combination for type 1 endometrial cancer (grades 1, 2 and 3), whereas for type

42 ncer (HR 0.59, 95% CI 0.36, 0.97, P = 0.04), endometrial cancer (HR 0.50, 95% CI 0.37, 0.67, P < 0.00

43 95% confidence interval (CI), 0.65-0.81] and endometrial cancer (OR = 0.68; 95% CI, 0.62-0.75), an as

44 s Radiotherapy Alone in Women With High-Risk Endometrial Cancer (PORTEC-3) trial investigated the ben

45 ncer (grades 1, 2 and 3), whereas for type 2 endometrial cancer (serous and carcinosarcoma), UBC, MRP

46 ndometrial biopsies obtained from women with endometrial cancer (type 1 or type 2) and without cancer

47 re aged 18 years or older and had metastatic endometrial cancer (unselected for microsatellite instab

48 Endometrial cancer accounts for ~76,000 deaths among wom

49 The incidence of endometrial cancer among younger women has been rising d

50 the increasing number of new diagnoses make endometrial cancer an important consideration in women's

51 Tamoxifen was associated with higher risk of endometrial cancer and cataracts compared with placebo.

52 echanisms underlying ER's regulatory role in endometrial cancer are poorly understood.

53 nosed with histologically confirmed invasive endometrial cancer between 2002 and 2006 and observed to

54 y mass index eliminated the association with endometrial cancer but had limited effect on other cance

55 ysical activity and survival in survivors of endometrial cancer by physical activity domain, intensit

56 fter a median follow-up of 17.9 years, 1,435 endometrial cancer cases and 904 ovarian cancer cases ha

57 different human BC cell lines and one human endometrial cancer cell line, and results were compared

58 Here, nine endometrioid endometrial cancer cell lines with PIK3A, PTEN, and KRAS

59 cellular and in vivo systems, colorectal and endometrial cancer cell lines, and biochemical and cellu

60 associated with docetaxel resistance in nine endometrial cancer cell lines.

61 t microsatellite stable (MSS) colorectal and endometrial cancer cell lines.

62 bility and proliferation in both ovarian and endometrial cancer cell lines.

63 Using breast and endometrial cancer cell models, EIS was then used to mon

64 nts on BET protein amounts in human Ishikawa endometrial cancer cells and patient-derived cell lines

65 Different gene mutations in endometrial cancer cells have varied responses to antica

66 oration of wild-type PPP2R1A in P179R-mutant endometrial cancer cells increases phosphatase activity

67 Restoring Cx43 expression in endometrial cancer cells reduced cellular migration; con

68 n factors that control ER genomic binding in endometrial cancer cells remain unknown.

69 ile causing additional regulatory changes in endometrial cancer cells that are distinct from breast c

70 ate factor controlling ER genomic binding in endometrial cancer cells, and here we explore the functi

71 Among PTEN mutations in endometrial cancer cells, the Y68 frame shift mutation o

72 s an important role in estrogen signaling in endometrial cancer cells.

73 rolling the activity of ER and the growth of endometrial cancer cells.

74 In an endometrial cancer cohort (n = 141), DNA hypermethylatio

75 .5 years, there were 60 deaths, including 18 endometrial cancer deaths, and 80 disease-free survival

76 rocession of neoplastic change that leads to endometrial cancer is initiated early in life.

77 umerous endocrine-resistant BC models and an endometrial cancer model and their molecular mechanisms

78 , we introduced the D538G mutation, a common endometrial cancer mutation that alters the ligand bindi

79 es reveal that adipose-derived stem cells in endometrial cancer pathogenesis influence epigenetic rep

80 guide prognosis and treatment decisions for endometrial cancer patients, while ongoing studies are e

81 al (p = 1.68 x 10-5, hazard ratio = 2.62) of endometrial cancer patients.

82 educing PP2A phosphatase activity to promote endometrial cancer progression.

83 s the protective association for ovarian and endometrial cancer remained significant up to 35 years a

84 Endometrial cancer remains the most common gynecological

85 However, its impact on endometrial cancer remains unclear.

86 mportance of a healthy lifestyle in lowering endometrial cancer risk among postmenopausal women.

87 en receptor alpha (ER) plays a major role in endometrial cancer risk and progression, however, the mo

88 f gene expression at the transcript level in endometrial cancer studies especially for types 1 and 2

89 tiated, poorly differentiated, and localized endometrial cancer than those in the lowest quintile (fo

90 ed the role of the tumor suppressor Fbxw7 in endometrial cancer through defined genetic model systems

91 d to Fbxw7 as a key driver of this enigmatic endometrial cancer type.

92 inoma and squamous cell carcinoma, liver and endometrial cancer were also observed, but the majority

93 phase 3 PORTEC-3 trial, women with high-risk endometrial cancer were eligible if they had Internation

94 activity in patients with advanced recurrent endometrial cancer with a safety profile that was simila

95 r older with breast, gastric, urothelial, or endometrial cancer with at least HER2 immunohistochemist

96 ing one deep vein thrombosis and one stage I endometrial cancer with tamoxifen and one pulmonary embo

97 s: RCC, 63% (19/30; 95% CI, 43.9% to 80.1%); endometrial cancer, 52% (12/23; 95% CI, 30.6% to 73.2%);

98 ents, coronary heart disease events, stroke, endometrial cancer, and cataracts; and mortality.

99 ncers, such as postmenopausal breast cancer, endometrial cancer, and colon cancer.

100 phyromonas somerae, a microbe of interest in endometrial cancer, as a proof-of-concept demonstration

101 In endometrial cancer, ESR1 mutations are associated with w

102 served in various cancers, including glioma, endometrial cancer, ovarian cancer, and breast cancer.

103 tase and tensin homolog), is well studied in endometrial cancer, recent studies suggest that DICER1,

104 s had metastatic renal cell carcinoma (RCC), endometrial cancer, squamous cell carcinoma of the head

105 matically reduce women's risk of ovarian and endometrial cancer, whereas their effect on lifetime ris

106 th a broader spectrum of cancers, especially endometrial cancer.

107 radiotherapy alone for women with high-risk endometrial cancer.

108 a preventive strategy for obesity-associated endometrial cancer.

109 ether account for over half of deaths due to endometrial cancer.

110 cellular communication in obesity-associated endometrial cancer.

111 nd five (39%, 13.9-68.4) of 13 patients with endometrial cancer.

112 A P179R as a biological driver of aggressive endometrial cancer.

113 r, GREB1 loss may predict chemoresistance of endometrial cancer.

114 therapy-resistant breast cancer and primary endometrial cancer.

115 as moderate efficacy in biomarker-unselected endometrial cancer.

116 s recapitulated in an obesity mouse model of endometrial cancer.

117 value for survival outcomes in patients with endometrial cancer.

118 iated with improved survival in survivors of endometrial cancer.

119 o influence the risk of breast, ovarian, and endometrial cancer.

120 gen receptor alpha (ER) is a key oncogene in endometrial cancer.

121 d effective precision therapy for aggressive endometrial cancer.See related article by Taylor et al.,

122 of Gynecology and Obstetrics (FIGO) stage II endometrial cancer: a 12-cm grade 3 endometrioid adenoca

123 and/or tumor mutational burden-high (TMB-H) endometrial cancers (ECs).

124 marize the overarching molecular features of endometrial cancers and highlight recent studies assessi

125 Transcriptomic analyses on endometrial cancers and precursors derived from these mo

126 Endometrial cancers are associated with several critical

127 Most endometrial cancers are carcinomas, with the remainder b

128 es, similar to published human DICER1-mutant endometrial cancers from TCGA (The Cancer Genome Atlas).

129 About one-third of these aggressive endometrial cancers harbor mutations in the protein phos

130 effects of higher testosterone on breast and endometrial cancers in women and prostate cancer in men.

131 ore resistant to chemotherapy and that human endometrial cancers with low GREB1 expression predict po

132 chanistic significance in the development of endometrial cancers, and suggest novel approaches for id

133 ent of more effective therapy for aggressive endometrial cancers, including uterine serous cancer and

134 mutations have been identified in breast and endometrial cancers, our finding may open a path towards

135 Similar to human endometrial cancers, tumors exhibited dysregulation of e

136 which is commonly upregulated in ovarian and endometrial cancers.

137 r and that are many-fold lower than those of endometrial cancers.

138 nature similar to those of human ovarian and endometrial cancers.

139 h frequencies of ~5-8% in colon, stomach and endometrial cancers.

140 sequencing data from 879 colon, stomach and endometrial cancers.

141 ice of therapy and prognosis in cervical and endometrial cancers; therefore, the exploration of senti

142 Endometrial carcinoma (EC) is a cancer type in which p53

143 ew York, we identified 843 women with occult endometrial carcinoma and 334 women with occult uterine

144 pecific PP2A PPP2R1A mutation as a driver of endometrial carcinoma and a target for novel therapeutic

145 e carcinosarcoma is an aggressive variant of endometrial carcinoma characterized by unusual histologi

146 vation as a critical component of high-grade endometrial carcinoma disease pathogenesis.

147 Patients with advanced endometrial carcinoma have limited treatment options.

148 c mutation site P179 facilitates features of endometrial carcinoma malignancy has yet to be fully det

149 s results for a patient cohort with advanced endometrial carcinoma receiving lenvatinib plus pembroli

150 most frequently altered gene in endometrioid endometrial carcinoma tumors is PTEN.

151 cutoff, 108 patients with previously treated endometrial carcinoma were enrolled, with a median follo

152 antitumor activity in patients with advanced endometrial carcinoma who have experienced disease progr

153 plus pembrolizumab in patients with advanced endometrial carcinoma, after establishing the maximum to

154 Among women with occult endometrial carcinoma, there was no significant associat

155 of tumor types, including bladder, lung, and endometrial carcinoma, we determined genes that are freq

156 biological basis by which the most recurrent endometrial carcinoma-specific mutation site P179 facili

157 ne PPP2R1A is highly prevalent in high-grade endometrial carcinoma.

158 Endometrial carcinomas can be classified into several hi

159 nt thoracic sarcomas(6) and dedifferentiated endometrial carcinomas(7).

160 aracterization of 95 prospectively collected endometrial carcinomas, comprising 83 endometrioid and 1

161 k of multiple cancers notably colorectal and endometrial carcinomas.

162 We profiled the behavior of seven endometrial cell types, including a previously uncharact

163 xtensive phenotypic analyses of HIV-infected endometrial cells by CyTOF, and use a 'nearest neighbor'

164 te into rare populations of nonhematopoietic endometrial cells in the uterus.

165 were observed between BRG1 and ARID1A mutant endometrial cells in vivo, including loss of epithelial

166 hich when blocked promotes death of infected endometrial cells.

167 l mutations shared among patients with MSI-H endometrial, colorectal, and stomach cancers.

168 ating a critical role for innate immunity in endometrial control of C. trachomatis infection.

169 associated with the presence of extrauterine endometrial cysts.

170 kingly, THC also inhibits the development of endometrial cysts.

171 s the role of enhancer of zeste homolog 2 in endometrial development.

172 Because endometrial disorders are also associated with aberrant

173 egulated decidualization in preeclampsia and endometrial disorders revealed by microarray data integr

174 pare the molecular pathologies of PE-CVS and endometrial disorders, as well as decidua obtained postp

175 hanging in the same direction for PE-CVS and endometrial disorders, suggesting common molecular pathw

176 al uterine defects, autoimmune disorders and endometrial dysfunction.

177 ody of the uterus> 3.0cm and the presence of endometrial echoes were highly specific for identifying

178 Endometrial, endocervical and ectocervical polarized epi

179 loci TJP2 and PRKCA was observed in primary endometrial endometrioid tumors and was associated with

180 The cellular source of newly regenerated endometrial epithelia during a mouse estrous cycle or a

181 ity being a common feature in SWI/SNF mutant endometrial epithelia.

182 en bovine and human) was produced and bovine endometrial epithelial (bEECs) and stromal (bESCs) and h

183 Mice lacking endometrial epithelial Arid1a are severely sub-fertile d

184 We propose that ARID1A normally maintains endometrial epithelial cell identity by repressing mesen

185 uterine carcinosarcoma cell of origin is an endometrial epithelial cell that subsequently undergoes

186 evaluated in silico and in vitro using human endometrial epithelial cells (EEC) grown as monolayers o

187 the effects of ASCs on the transcriptome of endometrial epithelial cells (EEC) in an in vitro cocult

188 helial (bEECs) and stromal (bESCs) and human endometrial epithelial cells (hEECs) were cultured for 2

189 nality in modifying the transcriptome of the endometrial epithelial cells to facilitate receptivity t

190 , we analyze ARID1A(WT) and ARID1A(KO) human endometrial epithelial cells.

191 ne tissue loss and persistently generate all endometrial epithelial lineages, including the functiona

192 te and comprehensively analyze 3-dimensional endometrial epithelial organoid (EEO) cultures from huma

193 rovide a resident cellular supply that fuels endometrial epithelial regeneration.

194 s, elicits a transcriptional response in the endometrial epithelium in species with different implant

195 that monoallelic loss of ARID1A in the mouse endometrial epithelium is sufficient for vaginal bleedin

196 The endometrial epithelium of the uterus regenerates periodi

197 on also supports the regeneration of uterine endometrial epithelium post parturition.

198 n of Arid1a with Ltf-iCre in the adult mouse endometrial epithelium preserves the gland development w

199 r findings describe a role for ARID1A in the endometrial epithelium supporting early pregnancy establ

200 intain homeostasis and regeneration of mouse endometrial epithelium under physiological conditions.

201 rm biofilms, alter barrier properties of the endometrial epithelium, and ultimately impact colonizati

202 -specific effects of Prevotella on the human endometrial epithelium.

203 RCA4), the SWI/SNF catalytic subunit, in the endometrial epithelium.

204 eered to inactivate BRG1 specifically in the endometrial epithelium.

205 rucial role of SMAD2/3 in maintaining normal endometrial function and confirm the hormone-dependent n

206 e glands of the uterus, which are central to endometrial function and fertility.

207 ostpartum endometrial repair is critical for endometrial function.

208 Negative elongation factor is essential for endometrial function.

209 transcription of the Foxa2 gene required for endometrial gland function.

210 genome sequencing, we show that normal human endometrial glands are clonal cell populations with tota

211 Normal endometrial glands frequently carry 'driver' mutations i

212 Endometrial glands were observed embedded in uterine myo

213 These models exhibit reduced endometrial glands, features of posteriorization and imp

214 a arises from the uncontrolled growth of the endometrial glands, which is typically associated with u

215 SI-MS imaging allowed clear visualization of endometrial glandular and stromal regions within tissue

216 e useful to explore mechanisms that regulate endometrial homeostasis and uterine function.

217 FBR1/ALK5 in the endometrium is required for endometrial homeostasis, tumor suppression, and postpart

218 Endometrial hyperplasia worsened with age, and all Smad2

219 growth and function, and the development of endometrial hyperplasia.

220 ing-mimicking diet prevent tamoxifen-induced endometrial hyperplasia.

221 Smad2/3 cKO mice were infertile due to endometrial hyperproliferation observed as early as 6 we

222 nfection alone (n = 92) or both cervical and endometrial infection (n = 68).

223 tokines associated with differential odds of endometrial infection and reinfection risk, and multivar

224 ORgammat or T-bet became more susceptible to endometrial infection with C. trachomatis, suggesting a

225 (P <= .05) associated with decreased odds of endometrial infection.

226 To identify endometrial innate immune components that interact with

227 that mouse ILCs contribute significantly to endometrial innate immunity via an IFN-gamma-dependent e

228 deficient mice significantly compromised the endometrial innate immunity, demonstrating an important

229 , suggesting a role for group 3-like ILCs in endometrial innate immunity.

230 deficient mice significantly compromised the endometrial innate immunity.

231 d for ILC development, significantly reduced endometrial innate immunity.

232 es of solid tumours (bladder, breast, colon, endometrial, laryngeal, lung, melanoma, oral or orophary

233 ioeconomic impact defined by the presence of endometrial-like tissue ("lesions") outside the uterus.

234 cal disease characterized by the presence of endometrial-like tissue lesions outside of the uterus.

235 The endometrial lining of the uterine cavity is a highly dyn

236 l-survival rate for R0 resection was 48% for endometrial malignancy, 40.6% for ovarian, 49.4% for cer

237 ) revealed a molecular signature of impaired endometrial maturation (decidualization) before and duri

238 e tumour types were anal, biliary, cervical, endometrial, mesothelioma, neuroendocrine, salivary, sma

239 tin remodeling subunits are also observed in endometrial neoplasms.

240 metrial ARID1A loss to endometriosis-related endometrial non-receptivity.

241 ion of p53 amyloid aggregates in both EC and endometrial nontumor cell lines.

242 l cancers are primarily imported from either endometrial or fallopian tube epithelium.

243 2 in the majority of people with colorectal, endometrial or ovarian cancer.

244 4% (n = 523) had gynecological malignancies (endometrial, ovarian, cervical, and vaginal), 35.7% (n =

245 rmonal, and immunological factors as well as endometrial progenitor cells are implicated in developme

246 efects in implantation, decidualization, and endometrial receptivity from disruption of the LIF-STAT3

247 ouse relies on stem cell-maintained rhythmic endometrial regeneration.

248 meostasis, tumor suppression, and postpartum endometrial regeneration.

249 indicating that TGFbeta-mediated postpartum endometrial repair is critical for endometrial function.

250 hether IFN-gamma-producing ILCs also improve endometrial resistance to sexually transmitted C. tracho

251 s, we hypothesized that pausing might impact endometrial response by coordinating hormonal signals in

252 -mediated pausing is essential to coordinate endometrial responses and that disruption impairs uterin

253 Endometrial samples and ULF were collected post-mortem f

254 In endometrial samples from cu-IUD users, there were no gen

255 These findings were largely derived from endometrial samples obtained through a transcervical cat

256 ated the molecular microbial profiles of mid-endometrial samples obtained through hysterectomy and co

257 ve birth was 180 of 690 women (26.1%) in the endometrial-scratch group and 176 of 674 women (26.1%) i

258 e randomly assigned in a 1:1 ratio to either endometrial scratching (by pipelle biopsy between day 3

259 The median score for pain from endometrial scratching (on a scale of 0 to 10, with high

260 Endometrial scratching (with the use of a pipelle biopsy

261 Endometrial scratching did not result in a higher rate o

262 te that sperm sialic acids may interact with endometrial Siglecs and that these interactions facilita

263 sPE may be part of a biologic continuum of "endometrial spectrum disorders."-Rabaglino, M.

264 d xenograft (PDX) models of ovarian (ST070), endometrial (ST040) and triple negative breast cancers (

265 ts these cells and prevents the formation of endometrial stroma in rodents, suggesting a progenitor f

266 Because endometrial stromal cell decidualization is also critica

267 ribe the generation of an immortalized human endometrial stromal cell line that uses yellow fluoresce

268 sm, reduces lactate secretion, and abrogates endometrial stromal cell proliferation in a coculture mo

269 n decidualized telomerase-immortalized human endometrial stromal cells (dT-HESCs) following infection

270 Indeed, when preimplantation endometrial stromal cells are exposed to hypoxic conditi

271 e rapid proliferation and differentiation of endometrial stromal cells into decidual cells, is requir

272 ession has a major impact on the capacity of endometrial stromal cells to recruit CD8 cells.

273 NELF-B or NELF-E subunits in cultured human endometrial stromal cells, which inhibited decidualizati

274 Homeobox a11 (Hoxa11)-deficient mice, having endometrial stromal-specific defects precluding decidual

275 riosis is an inflammatory condition in which endometrial tissue grows in ectopic locations.

276 Characterized by abnormal growth of uterine endometrial tissue in other body areas, endometriosis ca

277 valent in women that is defined by growth of endometrial tissue outside the uterine cavity and lacks

278 The presence and growth of endometrial tissue outside the uterine cavity in endomet

279 Endometriosis is the presence of endometrial tissue outside the uterus.

280 a and increased C. trachomatis burden in the endometrial tissue, confirming that mouse ILCs contribut

281 retrograde menstruation and implantation of endometrial tissue, mostly into the peritoneal cavity.

282 pithelial invasion in the spread of abnormal endometrial tissue.

283 Molecular analyses of ectopic and eutopic endometrial tissues could lead to enhanced understanding

284 olecular profiles of 231 eutopic and ectopic endometrial tissues from 89 endometriosis patients.

285 ed by immunohistochemistry (IHC) staining in endometrial tissues from endometriosis or control patien

286 trachomatis recovered from vaginal swabs or endometrial tissues peaked on day 3 and then declined in

287 rs that are significantly altered in ectopic endometrial tissues when compared to eutopic tissues wer

288 ich contain endometriosis tissues and normal endometrial tissues.

289 ent work showed that the embryo modified the endometrial transcriptome in vivo.

290 have significantly different effects on the endometrial transcriptome, with the LNG-IUS transcriptom

291 cular and cellular characterization of human endometrial transformation across the menstrual cycle, p

292 iated cell type, during four major phases of endometrial transformation, and found characteristic sig

293 motes migration and invasion of PTEN-deleted endometrial tumor cells.

294 e controlled by Arid1a and have an impact on endometrial tumor development.

295 hts into how ARID1A inactivation accelerates endometrial tumor progression and dissemination, the maj

296 Gastrointestinal and endometrial tumors comprise a separate cluster for which

297 The endometrial tumors develop only in Alk5 cKO mice that ar

298 ggering long-term silencing of these loci in endometrial tumors of obese patients.

299 Finally, examination of DICER1 hotspot endometrial tumors reveals derepression of specific miRN

300 epithelial ovarian cancers (EOCs), cervical, endometrial tumors, and uterine sarcomas that are genomi