ライフサイエンスコーパス: endometrial cancer

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

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

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

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

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

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

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

8 ated as an alternative staging technique for endometrial cancer.

9 signing PIK3 pathway targeting strategies in endometrial cancer.

10 CTCF is frequently mutated in endometrial cancer.

11 rol acetate combination for the treatment of endometrial cancer.

12 tion associated with increased expression in endometrial cancer.

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

14 value for survival outcomes in patients with endometrial cancer.

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

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

17 ly replace lymphadenectomy in the staging of endometrial cancer.

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

19 enectomy in detecting metastatic disease for endometrial cancer.

20 roscopic hysterectomy for women with stage I endometrial cancer.

21 t common genetic aberrations in endometrioid endometrial cancer.

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

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

24 ective screening methodology or protocol for endometrial cancer.

25 processes and the pathogenesis of breast and endometrial cancer.

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

27 on of interest for genetic susceptibility to endometrial cancer.

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

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

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

31 ose tissue contribute to the pathogenesis of endometrial cancer.

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

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

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

35 ined from patients with tamoxifen-associated endometrial cancer.

36 easingly younger population of patients with endometrial cancer.

37 ght into the genetic and biological basis of endometrial cancer.

38 cy of progestin therapy for the treatment of endometrial cancer.

39 ases to survey the evolutionary landscape of endometrial cancer.

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

41 cancer and RR = 0.88, 95% CI = 0.85-0.92 for endometrial cancer.

42 nd mTOR inhibitors show clinical activity in endometrial cancer.

43 iated with improved survival in survivors of endometrial cancer.

44 r functions as a novel therapeutic option in endometrial cancer.

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

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

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

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

49 a preventive strategy for obesity-associated endometrial cancer.

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

51 cellular communication in obesity-associated endometrial cancer.

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

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

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

55 therapy-resistant breast cancer and primary endometrial cancer.

56 as moderate efficacy in biomarker-unselected endometrial cancer.

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

58 ble for patients with advanced and recurring endometrial cancers.

59 erapeutic approach for targeting ovarian and endometrial cancers.

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

61 which is commonly upregulated in ovarian and endometrial cancers.

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

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

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

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

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

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

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

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

70 atients with glioblastoma and urothelial and endometrial cancer (all with FGFR2 or FGFR3 translocatio

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

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

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

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

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

76 tatistically significant association between endometrial cancer and age at first and last live birth,

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

78 tes were highly conserved between breast and endometrial cancer and enriched in binding motifs for th

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

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

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

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

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

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

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

86 s with decreased risk for primary breast and endometrial cancers and increased risks for lung cancer,

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

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

89 proteins correlate with diseases, including endometrial cancers and Roberts syndrome.

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

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

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

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

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

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

96 Endometrial cancers are associated with several critical

97 Most endometrial cancers are carcinomas, with the remainder b

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

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

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

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

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

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

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

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

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

107 limus shows encouraging activity in advanced endometrial cancer but is associated with significant to

108 cule (EpCAM) has been implicated in advanced endometrial cancer, but its roles in this progression re

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

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

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

112 ltiple genome-wide association and follow-up endometrial cancer case-control datasets identified a no

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

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

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

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

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

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

119 encing data and DNA copy number data from 25 endometrial cancer cell lines to identify potential ther

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

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

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

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

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

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

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

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

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

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

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

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

132 ors secreted from CDH1-negative, TP53 mutant endometrial cancer cells induced normal macrophages to e

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

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

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

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

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

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

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

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

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

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

143 ith high TNMC and GRS1 had twice the risk of endometrial cancer compared to those low in both indices

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

145 at CCL2 is a potent effector of LKB1 loss in endometrial cancer, creating potential avenues for thera

146 .5 years, there were 60 deaths, including 18 endometrial cancer deaths, and 80 disease-free survival

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

148 t in various cancers, but their potential in endometrial cancer (EC) is unknown.

149 Endometrial cancer (EC) remains the most common malignan

150 sed to calculate colorectal cancer (CRC) and endometrial cancer (EC) risks.

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

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

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

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

155 (PI3K) pathway is frequently dysregulated in endometrial cancer (EC).

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

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

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

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

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

161 Endometrial cancer (EMCA) is a clinically heterogeneous

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

163 In endometrial cancer, ESR1 mutations are associated with w

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

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

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

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

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

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

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

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

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

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

174 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 Endometrial cancer is the most common gynaecological tum

197 Endometrial cancer is the most common gynecologic cancer

198 Endometrial cancer is the most common gynecologic malign

199 Endometrial cancer is the most common gynecological mali

200 Endometrial cancer is the most common malignancy of the

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

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

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

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

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

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

207 11.4 years (mean) of follow-up, 566 incident endometrial cancer occurrences were confirmed by medical

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

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

210 95% confidence interval (CI), 0.65-0.81] and endometrial cancer (OR = 0.68; 95% CI, 0.62-0.75), an as

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

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

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

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

215 l novel therapeutic target for the high-risk endometrial cancer patient population.

216 assessment of lymph node metastases (LNM) in endometrial cancer patients and for the assessment of en

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

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

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

220 ly and disease recurrence postoperatively in endometrial cancer patients.

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

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

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

224 educing PP2A phosphatase activity to promote endometrial cancer progression.

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

226 al cancer patients and for the assessment of endometrial cancer recurrence (ECR) after primary surgic

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

228 Risks of postmenopausal breast and endometrial cancer related to overweight duration were m

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

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

231 Endometrial cancer remains the most common gynecological

232 However, its impact on endometrial cancer remains unclear.

233 and PTEN genes in large intestine, lung, and endometrial cancers respectively, indicating that TP53 t

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

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

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

237 , RAD51C, PALB2 and MSH6 in AML, stomach and endometrial cancers, respectively).

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

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

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

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

242 es showed no significant association between endometrial cancer risk and tea consumption and a weak a

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

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

245 is no consensus recommendation for reducing endometrial cancer risk for women with a mismatch repair

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

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

248 The association between parity and endometrial cancer risk is inconsistent from observation

249 (>/= 10 pounds) was associated with a higher endometrial cancer risk than was stable weight, especial

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

251 armaceutical interventions aimed at reducing endometrial cancer risk, improving cancer outcomes, and

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

253 ify the association between hypertension and endometrial cancer risk.

254 stimulatory effects of rs2494737 increasing endometrial cancer risk.

255 ith a statistically significant reduction in endometrial cancer risk.

256 pulation in regard to hormonal influences on endometrial cancer risk.

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

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

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

260 Results from preclinical studies in endometrial cancer show that metformin reduces cellular

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

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

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

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

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

266 ancer survivors and two randomized trials in endometrial cancer survivors were identified.

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

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

269 associated with high risks of colorectal and endometrial cancer that is caused by pathogenic variants

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

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

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

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

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

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

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

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

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

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

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

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

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

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

284 Endometrial cancer was diagnosed in 10.8% (n = 88) of pa

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

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

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

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

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

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

291 In the PORTEC trials, patients with endometrial cancer were randomly assigned to postoperati

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

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

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

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

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

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

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

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

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