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

3 processes and the pathogenesis of breast and endometrial cancer.

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

5 on of interest for genetic susceptibility to endometrial cancer.

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

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

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

9 ose tissue contribute to the pathogenesis of endometrial cancer.

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

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

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

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

14 ined from patients with tamoxifen-associated endometrial cancer.

15 easingly younger population of patients with endometrial cancer.

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

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

18 ases to survey the evolutionary landscape of endometrial cancer.

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

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

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

22 nd mTOR inhibitors show clinical activity in endometrial cancer.

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

24 ated as an alternative staging technique for endometrial cancer.

25 with skin cancer, in 32 of 168 samples from endometrial cancer.

26 hose with FGFR2-non-mutated (FGFR2(non-mut)) endometrial cancer.

27 xposure is believed to be the major cause of endometrial cancer.

28 y may be associated with a decreased risk of endometrial cancer.

29 metastasis and drug resistance in aggressive endometrial cancer.

30 women were diagnosed with incident invasive endometrial cancer.

31 signing PIK3 pathway targeting strategies in endometrial cancer.

32 he effects of bisphosphonates on the risk of endometrial cancer.

33 rescreening results, 27 (11%) had FGFR2(mut) endometrial cancer.

34 factors were associated with a lower risk of endometrial cancer.

35 Self-reported diagnosis of endometrial cancer.

36 ivery of precision medicine to patients with endometrial cancer.

37 source of noninvasive imaging biomarkers for endometrial cancer.

38 transformation are not well characterized in endometrial cancer.

39 classify the major histological subtypes of endometrial cancer.

40 itional and newer genomic classifications of endometrial cancer.

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

42 CTCF is frequently mutated in endometrial cancer.

43 rol acetate combination for the treatment of endometrial cancer.

44 tion associated with increased expression in endometrial cancer.

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

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

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

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

49 ly replace lymphadenectomy in the staging of endometrial cancer.

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

51 enectomy in detecting metastatic disease for endometrial cancer.

52 roscopic hysterectomy for women with stage I endometrial cancer.

53 t common genetic aberrations in endometrioid endometrial cancer.

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

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

56 ective screening methodology or protocol for endometrial cancer.

57 erapeutic approach for targeting ovarian and endometrial cancers.

58 H19 exist in both primary human ovarian and endometrial cancers.

59 ot be sufficient to prevent estrogen-induced endometrial cancers.

60 ble for patients with advanced and recurring endometrial cancers.

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

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

63 EPA + DHA intake had a 79% increased risk of endometrial cancer (95% CI: 16%, 175%; P-trend = 0.026).

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

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

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

67 follow-up through 2009, 386 women developed endometrial cancer among 36,115 considered in the analys

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

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

70 Role of Postoperative Radiation Therapy for Endometrial Cancer: An ASTRO Evidence-Based Guideline" b

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

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

73 in patients with FGFR2-mutated (FGFR2(mut)) endometrial cancer and in those with FGFR2-non-mutated (

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

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

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

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

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

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

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

81 FR2 mutations are found in 10-16% of primary endometrial cancers and provide an opportunity for targe

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

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

84 and FOXA1 (breast cancer), SOX17 and FOXA2 (endometrial cancer), and NFE2L2, SOX2, and TP63 (squamou

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

86 Ps) at the HNF1B locus to be associated with endometrial cancer, and now report extensive fine-mappin

87 years, 6,658 invasive breast cancers, 1,198 endometrial cancers, and 735 ovarian cancers were report

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

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

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

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

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

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

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

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

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

97 ctive effects of both tea and coffee against endometrial cancer, but recent reports from prospective

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

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

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

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

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

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

104 udies have shown that loss of SALL4 inhibits endometrial cancer cell growth in vitro and tumorigenici

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

106 sis, ALDH could be used to enrich for CSC in endometrial cancer cell lines and primary tumors, as ill

107 increases in the uptake of [(3)H]choline in endometrial cancer cell lines compared with normal endom

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

109 Using ovarian and endometrial cancer cell lines, we observed that TM downr

110 status irrespective of the PIK3CA status in endometrial cancer cell lines.

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

112 ved O-ASCs increase NO levels in ovarian and endometrial cancer cells and promote proliferation in th

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

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

115 des the migration and invasion properties of endometrial cancer cells in vitro and their metastatic p

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

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

118 L4 expression can affect drug sensitivity of endometrial cancer cells to carboplatin.

119 gnal transducers CD126 and GP130 in ALDH(hi) endometrial cancer cells.

120 ically binds to the c-Myc promoter region in endometrial cancer cells.

121 ression inhibited glycolysis and survival of endometrial cancer cells.

122 inicopathologic data from a population-based endometrial cancer cohort, unselected for age or family

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

124 ing glioblastoma, breast cancer, ovarian and endometrial cancers, colon cancer and lung squamous cell

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

126 Newly diagnosed patients with endometrial cancer completed questionnaires after diagno

127 f breast, prostate, colorectal, ovarian, and endometrial cancers completed a mailed survey on cancer

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

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

130 Inflammation may be important in endometrial cancer development.

131 es and glycemic loads are protective against endometrial cancer development.

132 deregulated gene, previously known to drive endometrial cancer development.

133 ion Women Study of whom 4067 women developed endometrial cancer during 5.2 million person-years of fo

134 Type II ovarian cancer (OC) and endometrial cancer (EC) are generally diagnosed at an ad

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

136 Endometrial cancer (EC) remains the most common malignan

137 creening practice for Lynch syndrome (LS) in endometrial cancer (EC) remains unknown.

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

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

140 edispose to both colorectal cancer (CRC) and endometrial cancer (EC).

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

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

143 The underlying causes of endometrial cancer (EMC) are poorly understood, and trea

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

145 Inflammation plays an important role in endometrial cancer etiology.

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

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

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

149 line chemotherapy for advanced or metastatic endometrial cancer from 46 clinical sites in seven count

150 Endometrial cancers from 702 patients recruited into the

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

152 However, patients with rectal or endometrial cancer had an increased probability of devel

153 t) and FGFR2(non-mut) advanced or metastatic endometrial cancer had single-agent activity, although i

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

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

156 one was associated with an increased risk of endometrial cancer (hazard ratio (HR) = 1.80, 95% confid

157 or example, we identified both known and new endometrial cancer hotspots in the tyrosine kinase domai

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 AEA concentrations observed in patients with endometrial cancer is a counter mechanism against furthe

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

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

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

178 ation of patients with MMR mutation-positive endometrial cancer is optimized by stepwise testing for

179 osis for women with recurrent and metastatic endometrial cancer is poor, and improved therapies are n

180 Endometrial cancer is the most common gynaecological tum

181 Endometrial cancer is the most common gynecologic cancer

182 Endometrial cancer is the most common gynecologic malign

183 Endometrial cancer is the most common gynecologic malign

184 Endometrial cancer is the most common gynecological mali

185 Endometrial cancer is the most common malignancy of the

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

187 as specific to women's cancers, specifically endometrial cancer, is scarce.

188 In human primary endometrial cancers, loss of LKB1 protein was strongly a

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

190 To test whether targeting endometrial cancer metabolism could be exploited as a th

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

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

193 Incident endometrial cancers (n = 263) were identified through th

194 usal women (mean follow-up: 10.8 years), 301 endometrial cancers occurred.

195 11.4 years (mean) of follow-up, 566 incident endometrial cancer occurrences were confirmed by medical

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

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

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

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

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

201 specifically present in RNA-Seq samples from endometrial cancer patients from TCGA, a virus not previ

202 Comparing 482 endometrial cancer patients with 571 population controls

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

204 ly and disease recurrence postoperatively in endometrial cancer patients.

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

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

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

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

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

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

211 verse association between parity and risk of endometrial cancer (relative risk (RR) for parous versus

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

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

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

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

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

217 bisphosphonates was associated with reduced endometrial cancer risk (adjusted hazard ratio, 0.80; 95

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

219 sahexaenoic acids) had significantly reduced endometrial cancer risk (HR: 0.59; 95% CI: 0.40, 0.82; P

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

221 we showed no significant association between endometrial cancer risk and consumption of either tea (m

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

223 controls, we found TNMC was associated with endometrial cancer risk and that the association remaine

224 t inverse associations were detected between endometrial cancer risk and total available carbohydrate

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

226 evidence for a single signal associated with endometrial cancer risk at the HNF1B locus, and that ris

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

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

229 Endometrial cancer risk has been directly associated wit

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

231 ship between use of oral bisphosphonates and endometrial cancer risk in a cohort of 89,918 postmenopa

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

233 We investigated endometrial cancer risk in relation to tea and coffee co

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

235 n omega-3 intake was associated with reduced endometrial cancer risk only in normal-weight women.

236 takes of LComega-3PUFAs were associated with endometrial cancer risk overall and stratified by body s

237 (>/= 10 pounds) was associated with a higher endometrial cancer risk than was stable weight, especial

238 s provide no evidence of further independent endometrial cancer risk variants at this locus.

239 t to the involvement of estrogen exposure in endometrial cancer risk with regard to genetic backgroun

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

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

242 ass is associated with both inflammation and endometrial cancer risk, it may modify the association o

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

244 stimulatory effects of rs2494737 increasing endometrial cancer risk.

245 ith a statistically significant reduction in endometrial cancer risk.

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

247 d menopause, are found to be associated with endometrial cancer risk.

248 associated with 15-23% linear reductions in endometrial cancer risk.

249 r no association between tea consumption and endometrial cancer risk.

250 elationship between the number of parity and endometrial cancer risk.

251 to more accurately estimate their effects on endometrial cancer risk.

252 individual omega-3 fatty acids and fish with endometrial cancer risk.

253 ments and intake of fish are associated with endometrial cancer risk.

254 ify the association between hypertension and endometrial cancer risk.

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

256 errantly expressed in 47.7% of primary human endometrial cancer samples.

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

258 ion of Ccl2 in an Lkb1-driven mouse model of endometrial cancer slowed tumor progression and increase

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

260 ients recruited into the Australian National Endometrial Cancer Study (ANECS) were tested for MMR pro

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

262 ning magnetic resonance mass spectroscopy on endometrial cancer surgical specimens and normal endomet

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

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

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

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

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

268 In endometrial cancers, the CPQ-PRKDC fusion transcript may

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

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

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

272 DC fusion transcript in three of 122 primary endometrial cancer tissues.

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

274 assisting a range of medical conditions from endometrial cancer to uterine bleeding and as an importa

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

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

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

278 mean age, 64 years; range, 24-91 years) with endometrial cancer underwent preoperative MR imaging, in

279 herapy may differentially affect the risk of endometrial cancer, using data from the Etude Epidemiolo

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

281 Endometrial cancer was diagnosed in 11% (n = 70) of wome

282 Endometrial cancer was diagnosed in 133 women (incidence

283 Endometrial cancer was diagnosed in 8.7% (n = 70) of wom

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

285 In order to assess their combined effects on endometrial cancer, we created the total number of menst

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

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

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

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

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

291 3 y of follow-up, n = 1253 incident invasive endometrial cancers were identified.

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

293 rtaken in women with metastatic or recurrent endometrial cancer who had progressive disease following

294 samples from 32 patients with colorectal or endometrial cancer who participated in Lynch syndrome sc

295 Recently, patients with endometrial cancer whose tumors expressed high levels of

296 ipid metabolism was severely dysregulated in endometrial cancer with various amino acids, inositols,

297 Patients with colon or endometrial cancers with MMR deficiency not explained by

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

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

300 that 3-bromopyruvate impaired the growth of endometrial cancer xenografts.