ライフサイエンスコーパス: endometrial carcinoma

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

2 urrent Rheb Tyr35Asn mutations in kidney and endometrial carcinoma.

3 latin in patients with advanced or recurrent endometrial carcinoma.

4 are all associated with PCOS as well as with endometrial carcinoma.

5 n active agent for the treatment of advanced endometrial carcinoma.

6 families with multiple members affected with endometrial carcinoma.

7 oxifene will increase the risk of developing endometrial carcinoma.

8 d estimates of the incidence of MI+ sporadic endometrial carcinoma.

9 Oral MPA is active against endometrial carcinoma.

10 trial hyperplasia (AEH) type with coexisting endometrial carcinoma.

11 inite activity against advanced or recurrent endometrial carcinoma.

12 , nor in Ishikawa cells derived from a human endometrial carcinoma.

13 development of the two most common types of endometrial carcinoma.

14 the pathogenesis of the endometrioid type of endometrial carcinoma.

15 metrioid carcinomas, the most common type of endometrial carcinoma.

16 f endocrine therapy in advanced or recurrent endometrial carcinoma.

17 ings had polyps, one of which had a focus of endometrial carcinoma.

18 nd aggressive features such as metastasis in endometrial carcinoma.

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

20 ressor PTEN is the most common alteration in endometrial carcinoma.

21 of external pelvic radiation in early-stage endometrial carcinoma.

22 current lesion in uterine carcinosarcoma and endometrial carcinoma.

23 he inhibitory subunit of PI3K, is mutated in endometrial carcinoma.

24 lia in this model was sufficient to initiate endometrial carcinoma.

25 ating FGFR2 as a novel therapeutic target in endometrial carcinoma.

26 specific marker of subsequent progression to endometrial carcinoma.

27 apies in patients with advanced or recurrent endometrial carcinoma.

28 I predicts the clinicopathologic features of endometrial carcinoma.

29 prostate intraepithelial neoplasia (PIN) and endometrial carcinoma.

30 ents with disseminated and high-risk limited endometrial carcinoma.

31 l target for the prevention and treatment of endometrial carcinoma.

32 in vitro model of well-differentiated human endometrial carcinoma.

33 ressor gene occur in approximately 30-50% of endometrial carcinomas.

34 sis in this large population-based series of endometrial carcinomas.

35 intestinal cancers are also disrupted in MI+ endometrial carcinomas.

36 bility (MSI) phenotype in sporadic colon and endometrial carcinomas.

37 wn MMR genes are infrequent in MSI+ sporadic endometrial carcinomas.

38 tumor suppressor gene occurs in about 40% of endometrial carcinomas.

39 ssociated with the MSI phenotype in sporadic endometrial carcinomas.

40 cription in hormonally responsive breast and endometrial carcinomas.

41 0q has been reported in approximately 40% of endometrial carcinomas.

42 n over 18% of colorectal adenocarcinomas and endometrial carcinomas.

43 ung squamous, head and neck, colorectal, and endometrial carcinomas.

44 omas, and in 1 of 266 epithelial ovarian and endometrial carcinomas.

45 levels in metastasizing and nonmetastasizing endometrial carcinomas.

46 serous cystadenocarcinoma and uterine corpus endometrial carcinomas.

47 he head and neck, melanomas, and ovarian and endometrial carcinomas.

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

49 48%) of 40 gastric carcinomas, 6 (33%) of 18 endometrial carcinomas, 14 (26%) of 51 of colorectal car

50 , 8 invasive ovarian carcinomas (15%), and 9 endometrial carcinomas (19%).

51 lence of Lynch syndrome in patients with LUS endometrial carcinoma (29%) is much greater than that of

52 or types, including colorectal, gastric, and endometrial carcinomas, also exhibit MI in a significant

53 ypes I (n = 1,312) and II (n = 138) incident endometrial carcinoma among 114,409 women in the Nationa

54 46% of patients (six of 13) with measurable endometrial carcinoma and 50% of patients (eight of 16)

55 precancers persist in uteri of patients with endometrial carcinoma and are monoclonal.

56 Doxorubicin and cisplatin have activity in endometrial carcinoma and at initiation of this study ra

57 ostate, colorectal, hepatocellular, lung and endometrial carcinoma and collecting duct carcinoma of t

58 demonstrated modest activity at best against endometrial carcinoma and does not warrant further inves

59 ameshift mutation in MSH3 was observed in an endometrial carcinoma and in an endometrial carcinoma ce

60 n of PTEN tumor suppressor gene is common in endometrial carcinoma and its precursor, atypical endome

61 udies of patients with advanced or recurrent endometrial carcinoma and no previous systemic therapy,

62 fferent human tumors including glioblastoma, endometrial carcinoma and prostate carcinoma.

63 Particularly, Akt1 deficiency inhibits endometrial carcinoma and prostate neoplasia in Pten(+/-

64 ocumented recurrent or persistent measurable endometrial carcinoma and with failure of one prior trea

65 Nineteen of 20 (95%) endometrial carcinomas and 8 of 8 (100%) benign endometr

66 d treated similarly to high-grade epithelial endometrial carcinomas and are no longer considered uter

67 enotype is present in a minority of sporadic endometrial carcinomas and is associated with high grade

68 (18)F-FDG PET/CT for preoperative staging in endometrial carcinomas and to investigate whether (18)F-

69 us cell carcinoma, hepatocellular carcinoma, endometrial carcinoma, and breast cancer.

70 whether HOXA10 expression is deregulated in endometrial carcinomas, and how counteracting this aberr

71 the PI3K pathway is extensively activated in endometrial carcinomas, and that combination of PIK3CA/P

72 Although both colorectal carcinoma and endometrial carcinoma are the most frequent component ca

73 ition, a minority of sporadic colorectal and endometrial carcinomas are RER positive.

74 8 cases, who were diagnosed with EH and then endometrial carcinoma at least 1 year later (median, 6 y

75 ospective cohort of 473 patients treated for endometrial carcinoma at this institution was identified

76 At combined endometrial carcinoma/atypical adenomatous hyperplasia p

77 ions with 31% or less combined prevalence of endometrial carcinoma/atypical adenomatous hyperplasia,

78 some 10 is implicated in the pathogenesis of endometrial carcinoma based on loss of heterozygosity (L

79 High-dose MA is active in endometrial carcinoma, but appears to have no advantage

80 otype has been reported in 9-43% of sporadic endometrial carcinomas, but there are conflicting data a

81 ndicates that the RER phenotype is common in endometrial carcinomas, but there is no association with

82 or HOXA10 deregulation in the progression of endometrial carcinoma by promoting epithelial-mesenchyma

83 In contrast, endometrial carcinoma cell growth in vitro and uterine e

84 RNA-mediated approach to knockdown CYP1B1 in endometrial carcinoma cell line followed by functional a

85 ma and their endometrial tissue and that the endometrial carcinoma cell line, Ishikawa, contains the

86 served in an endometrial carcinoma and in an endometrial carcinoma cell line.

87 Inhibition of FGFR2 kinase activity in endometrial carcinoma cell lines bearing such FGFR2 muta

88 otypic end points in two MMR-deficient human endometrial carcinoma cell lines that were originally is

89 on, we expressed wild-type or mutant PTEN in endometrial carcinoma cell lines.

90 AEA on the survival and proliferation of an endometrial carcinoma cell model.

91 ith Dr(+) E. coli was studied using Ishikawa endometrial carcinoma cells as an in vitro model of the

92 or growth, the ADM cDNA was transfected into endometrial carcinoma cells followed by xenografting int

93 Attenuation of CYP1B1 expression in endometrial carcinoma cells induces apoptosis and increa

94 Enforced expression of HOXA10 in endometrial carcinoma cells inhibited invasive behavior

95 CYP1B1 depletion in endometrial carcinoma cells leads to decreased cellular

96 major MMR gene, was restored in HEC59 human endometrial carcinoma cells or was present in adenovirus

97 ced a G(1) cell cycle arrest specifically in endometrial carcinoma cells that lack endogenous wild-ty

98 and mRNA expression in HUVECs, RL-95 (human endometrial carcinoma cells), OVCAR-3 (human ovarian ade

99 f the immortalized human hepatocytes but not endometrial carcinoma cells, even in the presence of an

100 ulates p27(KIP1) levels in some settings, in endometrial carcinoma cells, PTEN expression indirectly

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

102 n of 37 transcription factors in ovarian and endometrial carcinoma cells.

103 V40 immortalized human hepatocytes and human endometrial carcinoma cells.

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

105 es identified as differentially expressed in endometrial carcinoma, compared to those found by Cyber-

106 The incidence of endometrial carcinoma continues to escalate and, althoug

107 We speculate that CYP1B1 inhibition in endometrial carcinomas could be a useful therapeutic app

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

109 We found that 11 of 12 (91%) cases of endometrial carcinoma (EC) displaying MSI had hMLH1 prom

110 EN is involved in as high as 93% of sporadic endometrial carcinomas (EC), irrespective of microsatell

111 factor-beta (TGF-beta) signaling in primary endometrial carcinoma (ECA) cells leads to loss of TGF-b

112 1, endometrial epithelial cells derived from endometrial carcinomas (ECAs; n = 10) were unresponsive

113 Type II endometrial carcinomas (ECs) are estrogen independent, p

114 asia with or without atypia; 32 endometrioid endometrial carcinoma (EEC), including 20 low-grade (gra

115 Monoclonal lesions included endometrial carcinoma, endometrial polyps, and atypical

116 ded the two major histopathological types of endometrial carcinoma: endometrioid (n = 26; 14 microsat

117 We have previously shown that patients with endometrial carcinoma express elevated concentrations of

118 many endometrial carcinomas, we examined 70 endometrial carcinomas for alterations in PTEN/MMAC1.

119 A extracted from 109 formalin-fixed sporadic endometrial carcinomas for microsatellite instability.

120 s of the endometrium, we examined 32 primary endometrial carcinomas for mutations in PTEN.

121 ndometrial carcinoma, we screened 66 primary endometrial carcinomas for mutations in the helical and

122 mplex, and atypical (the direct precursor of endometrial carcinoma) for hMLH1 aberrant methylation.

123 current reports of the mutations observed in endometrial carcinomas from treated women, suggesting th

124 Importantly, the observation that endometrial carcinomas from women have a significant red

125 e basis of clinical and pathologic criteria, endometrial carcinoma has been distinguished as types I

126 and SIVmac251 to the apical surface of human endometrial carcinoma (HEC-1A) cells at pH 6.0 and 12 ho

127 ue-2 (hMSH2)-deficient and -proficient human endometrial carcinoma HEC59 cell lines to determine whet

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

129 Adding cisplatin to doxorubicin in advanced endometrial carcinoma improves RR and PFS with a negligi

130 pathway is sufficient for the initiation of endometrial carcinoma in naive adult uterine epithelia.

131 metrial gland hyperplasia that progresses to endometrial carcinoma in situ and endometrial adenocarci

132 Endometrial carcinoma in the lower uterine segment (LUS)

133 ential role of cdc25B in the pathogenesis of endometrial carcinomas in conjunction with ER-alpha.

134 phenotype is present in most colorectal and endometrial carcinomas in patients with the hereditary n

135 n situ (DCIS), 53 ovarian carcinomas, and 47 endometrial carcinomas in the second exon of WAF1/Cip1 (

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

137 fect on the incidence of prostate neoplasia, endometrial carcinoma, intestinal polyps and adrenal les

138 Traditional classification of endometrial carcinoma is based either on clinical and en

139 and estrogen signaling in the development of endometrial carcinoma is complex; the results presented

140 , and hyperestrogenism in the development of endometrial carcinoma is still controversial.

141 Endometrial carcinoma is the most common gynecological m

142 Endometrial carcinoma is the most common type of extraco

143 All six serous endometrial carcinomas lacked detectable mutations.

144 lines and in several primary tumours such as endometrial carcinomas, malignant melanoma and thyroid t

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

146 Previous loss-of-heterozygosity studies in endometrial carcinoma mapped a putative tumor suppressor

147 stologically confirmed advanced or recurrent endometrial carcinoma, measurable disease, no prior cyto

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

149 llite instability (MSI) has been detected in endometrial carcinomas occurring in women affected by he

150 Thirty-five (3.5%) of 1,009 women had endometrial carcinoma of the LUS.

151 outcomes in a large series of patients with endometrial carcinomas of the endometrioid type.

152 ges can help to distinguish most polyps from endometrial carcinomas on the basis of morphologic featu

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

154 ch to the treatment of advanced or recurrent endometrial carcinoma, particularly those lesions that a

155 s prospectively performed on 129 consecutive endometrial carcinoma patients.

156 ing the presence of lymph node metastases in endometrial carcinoma patients.

157 , analogous to those reported in ovarian and endometrial carcinoma, point to potential therapeutic av

158 Latent endometrial carcinoma precancers are normal-appearing en

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

160 e discovery of activating FGFR2 mutations in endometrial carcinoma raises the possibility of employin

161 estrogenic potency in Ishikawa cells (human endometrial carcinoma), rat uterine weight (systemic act

162 eligible patients with advanced or recurrent endometrial carcinoma received oral tamoxifen 20 mg bid

163 ar causes and consequences of MI in sporadic endometrial carcinomas remain obscure, however.

164 Endometrial carcinomas represent the most common gynecol

165 Endometrial carcinoma revealed no difference in staining

166 wth factor response element (EGFRE) in human endometrial carcinoma RL95-2 cells (RL95).

167 rin gene promoter in transiently transfected endometrial carcinoma RL95-2 cells.

168 of 40 samples, whereas none of the other 128 endometrial carcinoma samples were HPV38(+), raising dou

169 absence of the alteration at the 31st codon, endometrial carcinomas showed an increased percentage of

170 Immunohistochemical staining of endometrial carcinomas showed that CYP1B1 is up-regulate

171 that down-regulation of HOXA10 expression in endometrial carcinomas strongly correlates with increase

172 risk factor associations for Types I and II endometrial carcinomas, supporting the etiologic heterog

173 increased Amd1 expression in RNAs from mouse endometrial carcinomas that were hybridized to GeneChips

174 In endometrial carcinoma, the presence of MSI was independe

175 us staining protocols were applied to frozen endometrial carcinoma tissue sections.

176 n ideal platform for testing the response of endometrial carcinoma to targeted therapy against this c

177 ial assessed response rates in patients with endometrial carcinoma treated with high-dose MA.

178 fferent PR isoforms, PRA and PRB, in uterine endometrial carcinoma (UEC) using methylation-specific P

179 stimate the relative risk (RR) of developing endometrial carcinoma up to 25 years later.

180 ature of one of the most aggressive forms of endometrial carcinoma, uterine papillary serous cancer (

181 between polycystic ovary syndrome (PCOS)and endometrial carcinoma was first suggested in 1949, 14 ye

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

183 erall, mutations were detected in 50% of the endometrial carcinomas we analyzed.

184 As PTEN mutations occur at high frequency in endometrial carcinoma, we screened 66 primary endometria

185 cus is included in the region of LOH in many endometrial carcinomas, we examined 70 endometrial carci

186 the molecular basis of the role of CYP1B1 in endometrial carcinomas, we profiled the expression of ke

187 ty-three patients with recurrent or advanced endometrial carcinoma were entered into this Gynecologic

188 l and tumor DNA from 57 consecutive cases of endometrial carcinoma were examined for evidence of MI u

189 abolism that are differentially expressed in endometrial carcinoma were only found using this method.

190 ne eligible women with advanced or recurrent endometrial carcinoma were randomized to receive oral MP

191 f 25 patients who underwent hysterectomy for endometrial carcinoma were retrospectively evaluated.

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

193 Nine percent of the endometrial carcinomas were RER positive, and RER was si

194 ginal cuff in nine patients with cervical or endometrial carcinoma who underwent irradiation.

195 ivity in patients with advanced or recurrent endometrial carcinoma, who have not received systemic th

196 ty-four uterine serous carcinomas, a type of endometrial carcinoma with aggressive behavior and a hig

197 rated activity against advanced or recurrent endometrial carcinoma with response rates between 15% an

198 y were: (a) to identify a series of sporadic endometrial carcinomas with clear evidence of MI; (b) to

199 rognosis in a population-based series of 259 endometrial carcinomas with long-term follow-up.

200 t account for the great majority of sporadic endometrial carcinomas with MI and that a significant fr

201 Thus, we screened 16 endometrial carcinomas with microsatellite instability f

202 bnormalities are common in endometrioid type endometrial carcinomas with squamous differentiation.

203 promoter methylation and MSI status of those endometrial carcinomas with synchronous hyperplasias and

204 ne kinase gene, FGFR2, are present in 12% of endometrial carcinomas, with additional instances found