ライフサイエンスコーパス: endometrioid

1 gher in serous carcinoma tissues compared to endometrioid.

2 oengineered human endometrial tissue, termed endometrioid.

3 anced implantation efficiency in RIF-derived endometrioids.

4 increased risk of serous [1.13 (1.09-1.17)], endometrioid [1.20 (1.10-1.32)], and clear cell [1.37 (1

5 ding 6,179 of high-grade serous (HGS), 2,100 endometrioid, 1,591 mucinous, 1,034 clear cell, and 1,01

6 stment for LOC components [1.08 serous, 1.11 endometrioid, 1.26 clear cell, 0.94 mucinous].

7 epithelial ovarian cancer (2,045 serous, 319 endometrioid, 184 mucinous, 121 clear cell, 577 other/un

8 n cancers were identified (3,378 serous, 606 endometrioid, 331 mucinous, 269 clear cell, 1,000 other)

9 logies of interest (496 serous invasive, 139 endometrioid, 86 mucinous).

10 Rates of the most common gynecologic cancer, endometrioid adenocarcinoma (EAC), continue to rise, mir

11 ent tumors, we used a mouse model of ovarian endometrioid adenocarcinoma driven by concomitant activa

12 Endometrioid adenocarcinoma is the most frequent form of

13 erous carcinoma (43% and 29%), while grade 1 endometrioid adenocarcinoma showed the lowest levels (3%

14 stage II endometrial cancer: a 12-cm grade 3 endometrioid adenocarcinoma with 80% MMI and lymphovascu

15 Tumor histologic results included 39 endometrioid adenocarcinoma, 15 serous or clear cell, 3

16 l expression pattern typical of conventional endometrioid adenocarcinoma.

17 Cervical biopsy showed high-grade endometrioid adenocarcinoma.

18 frequently occurring histological subtype is endometrioid adenocarcinoma.

19 pical endometrial hyperplasia or endometrial endometrioid adenocarcinoma.

20 ical endometrial hyperplasia and endometrial endometrioid adenocarcinoma.

21 had surgery by a gynecologist, and 69.9% had endometrioid adenocarcinoma.

22 Roughly 40% of ovarian endometrioid adenocarcinomas (OEA) have constitutive act

23 Ovarian endometrioid adenocarcinomas (OEAs) frequently exhibit c

24 Prior studies have shown that ovarian endometrioid adenocarcinomas (OEAs) often carry mutation

25 hway, is deregulated in about 40% of ovarian endometrioid adenocarcinomas (OEAs), usually as a result

26 gulation are found in nearly half of ovarian endometrioid adenocarcinomas (OEAs).

27 ssion is elevated in human colon and ovarian endometrioid adenocarcinomas and mouse colon adenomas an

28 Specifically, in grade 3 endometrioid adenocarcinomas and uterine papillary serou

29 o produce mutant beta-catenin and in ovarian endometrioid adenocarcinomas characterized with respect

30 or gene at 10q25, we screened a panel of 123 endometrioid adenocarcinomas for loss of heterozygosity

31 In contrast, endometrioid adenocarcinomas show significant overlap wi

32 ssed in tumor-associated stroma of low-grade endometrioid adenocarcinomas, and (c) is aberrantly expr

33 olorectal carcinomas and a subset of ovarian endometrioid adenocarcinomas.

34 n, such as colorectal carcinomas and ovarian endometrioid adenocarcinomas.

35 e rate of 30% (95% CI, 14.7 to 49.4), all in endometrioid adenocarcinomas.

36 pithelial neoplasia) and well-differentiated endometrioid adenocarcinomas.

37 lected endometrial carcinomas, comprising 83 endometrioid and 12 serous tumors.

38 and tubal ligation were only associated with endometrioid and clear cell tumors (P-het </= .01).

39 PR and ER are prognostic biomarkers for endometrioid and high-grade serous ovarian cancers.

40 Endometrioid and low-grade serous carcinomas had similar

41 e particularly implicated in the etiology of endometrioid and mucinous carcinoma.

42 nedione associated with an increased risk in endometrioid and mucinous tumors [e.g., testosterone, en

43 For endometrioid and nonendometrioid EC, after adjusting for

44 erved difference in the MI frequency between endometrioid and serous carcinoma is statistically signi

45 The median B7-H4 concentration in endometrioid and serous histotypes was higher than in mu

46 PIK3CA, PPP2R1A, FBXW7, and KRAS, similar to endometrioid and serous uterine carcinomas.

47 ne non-serous epithelial ovarian tumors (six endometrioid and three mucinous) and their corresponding

48 ma has been distinguished as types I (mainly endometrioid) and II (nonendometrioid).

49 re recognized: the estrogen-related (type I, endometrioid) and the non-estrogen-related types (type I

50 athological subtypes are recognized: type I (endometrioid) and type II (nonendometrioid) carcinomas.

51 402 were serous, 74 were mucinous, 106 were endometrioid, and 127 were of other cell types.

52 sk factors and incidence of serous invasive, endometrioid, and mucinous ovarian cancers in the US Nur

53 subtypes suggested similar associations with endometrioid but not with mucinous or clear cell cancers

54 serous cancer (p = 0.018), and particularly endometrioid cancer (p = 0.0041), were seen with use of

55 e will define the precursor lesion of type I endometrioid cancer and the role of genetics and estroge

56 ion of endogenous MSX2 expression in ovarian endometrioid cancer cells carrying a beta-catenin mutati

57 r breast carcinoma and a stage IA clear cell endometrioid cancer confined to an endometrial polyp 6 y

58 rative analysis between CSCs and non-CSCs in endometrioid cancer models.

59 Despite stable incidence rates, endometrioid cancer mortality rates have not decreased o

60 was significantly elevated in clear cell and endometrioid cancer versus controls.

61 gh-grade serous ovarian cancer or high-grade endometrioid cancer, including primary peritoneal or fal

62 frequent mutations in ovarian clear cell and endometrioid cancers and in uterine endometrioid carcino

63 rly dysregulated in both nonendometrioid and endometrioid cancers relative to normal endometria.

64 s (13 serous papillary and 3 clear cell), 19 endometrioid cancers, and 7 age-matched normal endometri

65 24 transcripts could distinguish serous from endometrioid cancers, the two most common subgroups.

66 In human endometrioid cancers, we discovered that phosphorylated

67 a (HGSC), low-grade serous carcinoma (LGSC), endometrioid carcinoma (EC), clear cell carcinoma (CCC),

68 whereas complex hyperplasia and endometrial endometrioid carcinoma (EEC) had no or marginal expressi

69 n and uterine clear cell carcinoma (CCC) and endometrioid carcinoma (EMCA).

70 d with improved disease-specific survival in endometrioid carcinoma (log-rank p<0.0001) and high-grad

71 d with improved disease-specific survival in endometrioid carcinoma (log-rank p<0.0001).

72 ucinous (OR = 9.67; 95% CI = 1.10-84.80) and endometrioid carcinoma (OR = 3.41; 95% CI = 1.07-10.92),

73 c liability to polycystic ovary syndrome and endometrioid carcinoma (OR per 50% higher odds liability

74 1; P = 0.0003); age at natural menopause and endometrioid carcinoma (OR per year later onset: 1.09, 9

75 enetic alterations yet identified in uterine endometrioid carcinoma (UEC) are PTEN mutations and micr

76 from 4 women, 2 with HGSC and 2 with uterine endometrioid carcinoma (UEC) who were diagnosed as havin

77 tations occur with high frequency in uterine endometrioid carcinoma (UEC).

78 cantly improved disease-specific survival in endometrioid carcinoma compared with negative hormone-re

79 mutation MRE11(G285C) identified in uterine endometrioid carcinoma exhibited a similar cellular phen

80 endometrioid grades 1 and 2) and high-grade (endometrioid carcinoma International Federation of Gynec

81 In contrast, endometrioid carcinoma mortality rates remained stable.

82 Endometrioid carcinoma rates rose among non-Hispanic bla

83 Endometrioid carcinoma rates were highest in non-Hispani

84 inoma, 207 with mucinous carcinoma, 484 with endometrioid carcinoma, and 390 with clear-cell carcinom

85 ad-and-neck squamous cell carcinoma, uterine endometrioid carcinoma, and squamous cell carcinoma of t

86 an onco-miRNA that targets the PTEN gene in endometrioid carcinoma, its biological significance in B

87 encing showed the mouse BPRN tumors, but not endometrioid carcinoma-like tumors based on different ge

88 n stimulation in the pathogenesis of uterine endometrioid carcinoma.

89 all three histological grades of MI-positive endometrioid carcinoma.

90 ion status in 29 presumably sporadic uterine endometrioid carcinomas (UECs), which had previously bee

91 tumors are composed of mucinous carcinomas, endometrioid carcinomas, malignant Brenner tumors, and c

92 Previously we reported MI in 20% of uterine endometrioid carcinomas, the most common type of endomet

93 cell and endometrioid cancers and in uterine endometrioid carcinomas.

94 collected and analyzed for 446 patients with endometrioid carcinomas.

95 y implicated in the etiology of mucinous and endometrioid carcinomas.

96 PP2A subunit expression was rare in uterine endometrioid carcinomas.

97 ls show a close resemblance to human uterine endometrioid carcinomas.

98 , including clear cell, low-grade serous and endometrioid carcinomas.

99 erated decline, with the largest changes for endometrioid carcinomas.

100 ons were observed in 2 of 30 type I uterine (endometrioid) carcinomas (6.7%) and 5 of 26 type II uter

101 ed as were the carcinoma histotypes (serous, endometrioid, clear cell).

102 ervised clustering by risk factors separated endometrioid, clear cell, and low-grade serous carcinoma

103 i) endometriosis-related tumors that include endometrioid, clear cell, and seromucinous carcinomas; i

104 Less common epithelial subtypes include endometrioid, clear cell, low-grade serous, mucinous, an

105 (9.1%) including low-grade serous, low-grade endometrioid, clear-cell, and mucinous carcinomas.

106 P = .01), as was the proportion of tumors of endometrioid compared with nonendometrioid histologic su

107 Pik3ca), low-grade serous carcinoma (Braf), endometrioid (Ctnnb1), or mucinous (Kras) carcinomas.

108 d vaginal brachytherapy (VBT) in early-stage endometrioid EC (EEC).

109 trozole/abemaciclib/metformin in ER positive endometrioid EC (NCT03675893).

110 development of this combination in recurrent endometrioid EC is under way.

111 Patients with grade 2 endometrioid EC underwent pelvic lymphadenectomy (PLND)

112 t the data cutoff date, 30 patients (28 with endometrioid EC) initiated protocol therapy; 15 (50%) pa

113 vidence of activity in recurrent ER positive endometrioid EC.

114 d ratio [HR] = 1.07; 95% CI, 0.88-1.30) with endometrioid EC.

115 The most common histologies were endometrioid endometrial adenocarcinoma (n = 13), prosta

116 One patient with endometrioid endometrial adenocarcinoma achieved a CR an

117 Here, we describe a novel, adherent endometrioid endometrial cancer (EEC) cell line model, H

118 ificance of mismatch repair (MMR) defects in endometrioid endometrial cancer (EEC) has not been defin

119 Here, nine endometrioid endometrial cancer cell lines with PIK3A, P

120 Here we find that PTEN-deficient endometrioid endometrial cancer cells are not responsive

121 TEN depletion rendered PTEN wild-type Hec-1A endometrioid endometrial cancer cells responsive to comb

122 d GADD45alpha mRNA and protein expression in endometrioid endometrial cancer compared to normal endom

123 Hong Kong randomized 760 women with stage I endometrioid endometrial cancer to either TLH or TAH.

124 gnificance of ATR mutations in patients with endometrioid endometrial cancer.

125 ot associated with survival in patients with endometrioid endometrial cancer.

126 ost common malignant tumour of the uterus is endometrioid endometrial cancer.

127 h in a genetic mouse model of Pten-deficient endometrioid endometrial cancer.

128 ne of the most common genetic aberrations in endometrioid endometrial cancer.

129 pha, the catalytic subunit of PI3K, occur in endometrioid endometrial cancers (EEC) and nonendometrio

130 to expand the utility of PARP inhibitors to endometrioid endometrial cancers in a PTEN-deficient set

131 These data classify histologically similar endometrioid endometrial cancers into two distinct group

132 Analysis of 116 primary endometrioid endometrial cancers revealed that FGFR2 and

133 ak repair, vulnerabilities of PTEN-deficient endometrioid endometrial cancers to PARP inhibition rema

134 obal gene expression profiles of early-stage endometrioid endometrial cancers with and without the MS

135 t growth factor receptor 2 (FGFR2) in 16% of endometrioid endometrial cancers, we sought to determine

136 trial hyperplasia with or without atypia; 32 endometrioid endometrial carcinoma (EEC), including 20 l

137 nsideration in the management of early-onset endometrioid endometrial carcinoma (EEEC), particularly

138 No increased risk for endometrioid endometrial carcinoma or sarcoma was found

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

140 ial cancer cell lines (n = 6) and 68% of 117 endometrioid endometrial tumors analyzed.

141 thelium led to rapid development of advanced endometrioid endometrial tumors with 100% penetrance and

142 netic lesion in the estrogen-related type I (endometrioid) endometrial cancer.

143 mucinous EOC (3q22.3 and 9q31.1) and one for endometrioid EOC (5q12.3).

144 based chemotherapy with high-grade serous or endometrioid EOC should be offered PARPi maintenance the

145 istologic subtype: 93% of serous and 100% of endometrioid EOCs expressed HE4, whereas only 50% and 0%

146 oprotein that is overexpressed by serous and endometrioid EOCs.

147 expression decreased in late disease stage 4 endometrioid EOCs.

148 ith Platinum-Sensitive, High-Grade Serous or Endometrioid Epithelial Ovarian, Primary Peritoneal or F

149 astoid implantation capability compared with endometrioids from fertile controls.

150 ise to preneoplastic ovarian lesions with an endometrioid glandular morphology.

151 aecology and Obstetrics (FIGO) 2009 stage I, endometrioid grade 3 cancer with deep myometrial invasio

152 It classifies these slides into low-grade (endometrioid grades 1 and 2) and high-grade (endometrioi

153 tations were seen primarily in tumors of the endometrioid histologic subtype (18/115 cases investigat

154 The largest changes were found for the endometrioid histologic subtype.

155 , encompassing endocervical, intestinal, and endometrioid histological subtypes, and in nine of nine

156 majority of patients had low-grade (1 or 2) endometrioid histology (82%) and recurrences confined to

157 esda guidelines or Amsterdam II criteria) or endometrioid histology alone would have missed 9/16 (56%

158 Patients with endometrioid histology and CTNNB1 mutations responded we

159 logy and Obstetrics (FIGO) stage I/II of non-endometrioid histology or endometrioid histology with p5

160 stage I/II of non-endometrioid histology or endometrioid histology with p53/TP53 abnormality, or sta

161 RNRi gemcitabine compared with patients with endometrioid histology.

162 ed in the formation of precancerous lesions (endometrioid intraepithelial neoplasia) and well-differe

163 f 336 cases, 2.11, 1.39-3.20, p<0.0001), and endometrioid invasive ovarian cancers (169 [13.9%] of 12

164 , Hoxa10 and Hoxa11 induced morphogenesis of endometrioid-like and mucinous-like EOCs, respectively.

165 carcinoma (serous, clear cell, mucinous, and endometrioid) likely represent distinct disease entities

166 cancer including high and low grade serous, endometrioid, mucinous, clear cell, and granulosa cell c

167 pathological types of endometrial carcinoma: endometrioid (n = 26; 14 microsatellite instability (MI)

168 We classified endometrioid (n = 7,246), adenocarcinoma not otherwise s

169 as well as serous (n = 249), clear cell and endometrioid (n = 91), and mucinous (n = 144) EOC.

170 luded patients with clinical stage I grade 2 endometrioid or high-grade EC scheduled to undergo lapar

171 esistant, epithelial (ie, high-grade serous, endometrioid, or carcinosarcoma with a >=30% epithelial

172 d older with stage III/IV high-grade serous, endometrioid, or clear cell ovarian cancer in clinical c

173 en diagnosed with invasive serous, mucinous, endometrioid, or clear-cell carcinomas of the ovary.

174 Women diagnosed with clear cell, endometrioid, or mucinous ovarian cancer should be offer

175 netic models of peritoneal endometriosis and endometrioid ovarian adenocarcinoma in mice, both based

176 induction of invasive and widely metastatic endometrioid ovarian adenocarcinomas with complete penet

177 of this study was to further characterize an endometrioid ovarian cancer cell line, SNU-251, which wa

178 patients with relapsed high-grade serous or endometrioid ovarian cancer who were platinum sensitive

179 ly diagnosed, advanced, high-grade serous or endometrioid ovarian cancer with a complete or partial c

180 rent platinum-sensitive high-grade serous or endometrioid ovarian cancer, and warrants study in a pha

181 d, relapsed, high-grade serous or high-grade endometrioid ovarian cancer, including primary peritonea

182 ly diagnosed, advanced, high-grade serous or endometrioid ovarian cancer, primary peritoneal cancer,

183 Clear cell ovarian carcinoma (CCOC) and endometrioid ovarian carcinoma (ENOC) are ovarian carcin

184 Endometrioid ovarian carcinoma (EnOC) demonstrates subst

185 Mouse serous and endometrioid ovarian carcinoma cell lines were tested in

186 Endometrioid ovarian carcinomas are frequently associate

187 POLE proofreading domain mutations in three endometrioid ovarian tumors.

188 um-sensitive, relapsed, high-grade serous or endometrioid ovarian, fallopian tube, or primary periton

189 d a platinum-sensitive, high-grade serous or endometrioid ovarian, primary peritoneal, or fallopian t

190 had platinum-sensitive, high-grade serous or endometrioid ovarian, primary peritoneal, or fallopian t

191 Endometrioid OvCA (EOC) is a prototypical type I tumor,

192 measurable or evaluable high-grade serous or endometrioid platinum-sensitive recurrent ovarian cancer

193 her parity was most strongly associated with endometrioid (relative risk [RR] per birth, 0.78; 95% CI

194 nto several histological subtypes, including endometrioid, serous and clear cell carcinomas.

195 or on histopathological characteristics (eg, endometrioid, serous, or clear-cell adenocarcinoma).

196 decreased risk of clear cell, mucinous, and endometrioid subtype, but not with the most common serou

197 lasma samples, consistent with the fact that endometrioid tumor is the prevalent type in this species

198 T1a lesion (37 836 [66.9%]) and grade 1 or 2 endometrioid tumors (40 589 [71.8%]).

199 de (4) and high grade (5) serous tumors, and endometrioid tumors (6).

200 1.7, 95% confidence interval: 1.4, 2.2) and endometrioid tumors (IRR = 1.5, 95% confidence interval:

201 Risk factor patterns for high-grade endometrioid tumors and type II tumors were similar.

202 nd PRKCA was observed in primary endometrial endometrioid tumors and was associated with obesity.

203 Similar increased risks of serous and endometrioid tumors were found with estrogen/progestin t

204 Among all tumor types, endometrioid tumors were the most strongly related to pr

205 when the low-risk group (stage IA, grade 1-2 endometrioid tumors with no LVSI) was assessed per nodal

206 oid and mucinous tumors [e.g., testosterone, endometrioid tumors, ORlog2 = 1.40 (1.03-1.91)], but not

207 onetheless, MSI occurs almost exclusively in endometrioid tumors.

208 The median patient age was 63 years; 50% had endometrioid tumors.

209 mutations and microsatellite instability for endometrioid tumors.

210 %) MI-positive and 4 of 12 (33%) MI-negative endometrioid tumors.

211 rtunity to target both signaling pathways in endometrioid tumors.

212 ancers (3% and 1%), with similar results for endometrioid type (P < .0001).

213 rolonged survival specifically in high-grade endometrioid type and serous tumors.

214 beta-catenin abnormalities are common in endometrioid type endometrial carcinomas with squamous d

215 significant role in the pathogenesis of the endometrioid type of endometrial carcinoma.

216 PTEN mutations have been reported in the endometrioid type of uterine tumors which are associated

217 patients with endometrial carcinomas of the endometrioid type.

218 type than in cancers of the less-aggressive endometrioid type.

219 d/d) mice treated with E2 developed invasive endometrioid-type endometrial adenocarcinoma.

220 n status and expression of ARID1A protein in endometrioid-type endometrial tumors.

221 Smad2/3 cKO mice ultimately developed bulky endometrioid-type uterine cancers with 100% mortality by