ライフサイエンスコーパス: endometrioid

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

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

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

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

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

6 Endometrioid adenocarcinoma is the most frequent form of

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

8 frequently occurring histological subtype is endometrioid adenocarcinoma.

9 pical endometrial hyperplasia or endometrial endometrioid adenocarcinoma.

10 ical endometrial hyperplasia and endometrial endometrioid adenocarcinoma.

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

12 l expression pattern typical of conventional endometrioid adenocarcinoma.

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

14 Ovarian endometrioid adenocarcinomas (OEAs) frequently exhibit c

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

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

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

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

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

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

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

22 In contrast, endometrioid adenocarcinomas show significant overlap wi

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

24 olorectal carcinomas and a subset of ovarian endometrioid adenocarcinomas.

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

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

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

28 Endometrioid and low-grade serous carcinomas had similar

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

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

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

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

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

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

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

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

37 402 were serous, 74 were mucinous, 106 were endometrioid, and 127 were of other cell types.

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

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

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

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

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

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

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

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

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

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

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

49 24 transcripts could distinguish serous from endometrioid cancers, the two most common subgroups.

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

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

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

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

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

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

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

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

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

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

60 n stimulation in the pathogenesis of uterine endometrioid carcinoma.

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

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

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

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

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

66 cell and endometrioid cancers and in uterine endometrioid carcinomas.

67 collected and analyzed for 446 patients with endometrioid carcinomas.

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

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

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

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

72 (9.1%) including low-grade serous, low-grade endometrioid, clear-cell, and mucinous carcinomas.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 oprotein that is overexpressed by serous and endometrioid EOCs.

101 expression decreased in late disease stage 4 endometrioid EOCs.

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

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

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

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

106 Patients with endometrioid histology and CTNNB1 mutations responded we

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

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

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

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

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

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

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

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

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

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

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

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

119 Endometrioid ovarian carcinomas are frequently associate

120 POLE proofreading domain mutations in three endometrioid ovarian tumors.

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

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

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

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

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

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

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

128 1.7, 95% confidence interval: 1.4, 2.2) and endometrioid tumors (IRR = 1.5, 95% confidence interval:

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

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

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

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

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

134 mutations and microsatellite instability for endometrioid tumors.

135 %) MI-positive and 4 of 12 (33%) MI-negative endometrioid tumors.

136 rtunity to target both signaling pathways in endometrioid tumors.

137 onetheless, MSI occurs almost exclusively in endometrioid tumors.

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

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

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

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

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

143 patients with endometrial carcinomas of the endometrioid type.

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