ライフサイエンスコーパス: ESCC

1 ESCC miRNAs have a known role in regulating the unique e

2 ESCC risk was associated with nitrite intake (HR for 0.1

3 nalysis of 2,240 gastric cancer cases, 2,115 ESCC cases and 3,302 controls drawn from five studies.

4 NMDAR2B expression was silenced in all 12 ESCC cell lines and was reactivated by the demethylating

5 f primary human ESCC tissue specimens and 12 ESCC cell lines by sequence analysis.

6 exome sequencing on 51 tumor regions from 13 ESCC cases and multiregion global methylation profiling

7 (95%) showed reduced expression, and 9 of 13 ESCC cell lines were silenced for trypsinogen expression

8 5/60 tumor samples and 1/16 ESCC cell lines were positive for the EBV sequence.

9 ic copy number variations (SCNV) of over 180 ESCCs.

10 We identified 201 ESCC cases among 47,405 subjects.

11 th genes for the presence of mutations in 24 ESCC primary tumors and 16 tumor cell lines by directly

12 Three (11.5%) of 26 ESCCs exhibited NELL1 hypermethylation.

13 ome-wide scans that included a total of 2961 ESCC cases and 3400 controls.

14 C) in individuals of Chinese ancestry (5,337 ESCC cases and 5,787 controls) with 9,654 ESCC cases and

15 Conditioned media from a panel of 4 ESCC lines transdifferentiated normal esophageal fibrobl

16 ength/attrition in cancer/stroma cells in 47 ESCC patients.

17 sh samples from n = 81/160 EAC and n = 25/50 ESCC cases/matched controls.

18 ed the analysis of germ line samples from 50 ESCC patients and 50 matched controls.

19 37 ESCC cases and 5,787 controls) with 9,654 ESCC cases and 10,058 controls for follow-up.

20 In all, 70 ESCC patients (44 FH+ and 26 FH-) were examined by direc

21 mined for the mutations identified in the 70 ESCC patients.

22 tion between SNPs and FH of UGI cancer among ESCC cases in a stage-1 case-only analysis of the Nation

23 (-9); per-allele odds ratio (OR) = 1.31) and ESCC (P = 3.85 x 10(-9); OR = 1.34).

24 ophagogastric junctional adenocarcinoma, and ESCC) in the UK general population.

25 ome-wide significance for gastric cancer and ESCC independently.

26 ovel association between the gene CDKN2B and ESCC ([Formula: see text]).

27 h normal differentiated esophageal cells and ESCC, respectively.

28 C1-PE cells in three-dimensional culture and ESCC samples.

29 relationship of oral microbiota with EAC and ESCC risk in a prospective study nested in two cohorts.

30 he early detection and prevention of EAC and ESCC.

31 hether an association exists between EBV and ESCC.

32 he EGFR signaling pathway and risk of GC and ESCC.

33 cant associations between alcohol intake and ESCC risk (HR = 4.93, 95% CI: 2.69, 9.03) but not risk f

34 ed between N-nitrosodimethylamine intake and ESCC risk (HR for 0.1-mug/d increase in intake: 1.15; 95

35 ween GNAI3, CHRNE, PAK4, WASL, and ITCH, and ESCC (P<0.05).

36 ssue microarrays of esophageal neoplasms and ESCC as well as extracted tumor samples were stained for

37 scriptome sequence profiling of nontumor and ESCC clinical samples, we identified a subset of signifi

38 verexpressed in the majority of patients and ESCC cell lines.

39 ctive T cells, chronic fungal infection, and ESCCs expressing specific human ESCC markers.

40 this model, we investigated the link between ESCC and fungal infection.

41 t downregulation of Rab25 expression in both ESCC cell lines and clinical samples was associated with

42 NPs in 1116 esophageal squamous cell cancer (ESCC) patients and 1117 cancer-free controls to assess t

43 denocarcinoma (EAC) or squamous cell cancer (ESCC) present with advanced, incurable disease.

44 study of esophageal squamous cell carcinoma (ESCC) and detected a highly significant novel associatio

45 guishing esophageal squamous cell carcinoma (ESCC) and EAC from normal esophagus (NE) (P<0.001).

46 in both esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EACA) and 100% in m

47 risk of esophageal squamous cell carcinoma (ESCC) and gastric cardia adenocarcinomas (GCA) in common

48 rates of esophageal squamous cell carcinoma (ESCC) and gastric noncardia adenocarcinoma have decrease

49 nosis of esophageal squamous cell carcinoma (ESCC) are not well understood.

50 000 new oesophageal squamous-cell carcinoma (ESCC) cases each year occur in China.

51 ssion of esophageal squamous cell carcinoma (ESCC) causes a high mortality rate because of the propen

52 ified in esophageal squamous cell carcinoma (ESCC) cell lines, N-methyl-D-aspartate receptor type 2B

53 tosis in esophageal squamous cell carcinoma (ESCC) cells.

54 ly stage esophageal squamous cell carcinoma (ESCC) could improve clinical outcomes, when combined wit

55 role in esophageal squamous cell carcinoma (ESCC) has not been studied.

56 udies of esophageal squamous cell carcinoma (ESCC) have shown a high frequency of allelic loss on chr

57 al adeno- (EAC) and squamous cell carcinoma (ESCC) in Caucasians.

58 ncer and esophageal squamous cell carcinoma (ESCC) in ethnic Chinese subjects in which we genotyped 5

59 GWAS) on esophageal squamous cell carcinoma (ESCC) in Han Chinese, we conducted a follow-up study to

60 GWAS) of esophageal squamous cell carcinoma (ESCC) in individuals of Chinese ancestry (5,337 ESCC cas

61 ption in esophageal squamous cell carcinoma (ESCC) independent of adenomatous polyposis coli and beta

62 Esophageal squamous cell carcinoma (ESCC) is among the most common malignancies, but little

63 Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy with a poor prognosis

64 Esophageal squamous cell carcinoma (ESCC) is known to be a highly angiogenic tumor.

65 Esophageal squamous cell carcinoma (ESCC) is prevalent worldwide and particularly common in

66 Esophageal squamous cell carcinoma (ESCC) is the commonest primary malignant esophageal tumo

67 nesis of esophageal squamous cell carcinoma (ESCC) is thought to involve a combination of genetic and

68 of 1095 esophageal squamous cell carcinoma (ESCC) patients, including 679 in surgery alone group (gr

69 on in 50 esophageal squamous cell carcinoma (ESCC) primary tumors with well characterized clinicopath

70 nts with esophageal squamous cell carcinoma (ESCC) receiving chemoradiation.

71 ex vivo esophageal squamous cell carcinoma (ESCC) specimens and analyzed transcriptomes throughout t

72 study of esophageal squamous cell carcinoma (ESCC) that included the analysis of germ line samples fr

73 risk of esophageal squamous cell carcinoma (ESCC) which suggested a possible role for gastric microb

74 nts with esophageal squamous cell carcinoma (ESCC) with poor prognosis, and elevation of its expressi

75 and 110 esophageal squamous cell carcinoma (ESCC), 151 esophageal adenocarcinoma, 166 gastric cardia

76 EAC) and esophageal squamous cell carcinoma (ESCC), although evidence is limited to cross-sectional s

77 ntial in esophageal squamous cell carcinoma (ESCC), among the deadliest of all human carcinomas.

78 opsies of esophagus squamous cell carcinoma (ESCC), an aggressive tumor with poor prognosis, as compa

79 176 were esophageal squamous cell carcinoma (ESCC), and 23 were other types of esophageal cancer.

80 plified oesophageal squamous cell carcinoma (ESCC), but may become quickly ineffective.

81 subtype, esophageal squamous cell carcinoma (ESCC), is an aggressive cancer with poor prognosis due t

82 Esophageal squamous cell carcinoma (ESCC), the major histologic subtype of esophageal cancer

83 ility in esophageal squamous cell carcinoma (ESCC), we examined loss of heterozygosity (LOH), copy nu

84 ample is esophageal squamous cell carcinoma (ESCC), which is associated with a high mortality rate th

85 nts with esophageal squamous cell carcinoma (ESCC).

86 loci for esophageal squamous cell carcinoma (ESCC).

87 risk of esophageal squamous cell carcinoma (ESCC).

88 nesis of esophageal squamous cell carcinoma (ESCC).

89 PTTG1 in esophageal squamous cell carcinoma (ESCC).

90 tion and esophageal squamous cell carcinoma (ESCC).

91 2.11 for esophageal squamous cell carcinoma (ESCC).

92 pCR for esophageal squamous cell carcinoma (ESCC).

93 causes oesophageal squamous cell carcinoma (ESCC).

94 nesis of esophageal squamous cell carcinoma (ESCC).

95 risk of esophageal squamous cell carcinoma (ESCC).

96 odels of esophageal squamous cell carcinoma (ESCC).

97 ommon in esophageal squamous cell carcinoma (ESCC); however, the mechanisms underlying this instabili

98 ] and/or esophageal squamous cell carcinoma [ESCC]).

99 of 1126 esophageal squamous cell carcinomas (ESCC) patients and 1131 controls, we genotyped two SNPs

100 AT3) in esophageal squamous cell carcinomas (ESCC, n=49) and Barrett's adenocarcinomas (BAC, n=61) re

101 l or head and neck squamous cell carcinomas (ESCCs or HNSCCs, respectively) results in lower levels o

102 l in 49 esophageal squamous cell carcinomas (ESCCs) and 72 gastric adenocarcinomas.

103 or 1942 esophageal squamous cell carcinomas (ESCCs), 1758 gastric cancers (GCs), and 2111 controls.

104 ressing esophageal squamous cell carcinomas (ESCCs).

105 was significantly associated with decreased ESCC and GCA risk especially for the subjects with under

106 c corpus mucosal microbiota differs in early ESCC and ESD from healthy esophagus.

107 Cases were included subjects with early ESCC (stage I-II) and esophageal squamous dysplasia (ESD

108 We find that seven of eight ESCC lines tested are inhibited by p16 and fail to expre

109 We found a significantly elevated ESCC risk associated with the rs238406 T variant genotyp

110 Eleven ESCC cell lines expressed PTTG1 protein at levels 2.4 to

111 m an organotypic culture model of engineered ESCC.

112 squamous epithelial cells of the esophagus (ESCC).

113 a role in genetic susceptibility to familial ESCC.

114 For ESCC, we did not observe a significant pathway-level ass

115 utable risks of 77% (95% CI: 0.55, 0.89) for ESCC, 58% (95% CI: 0.38, 0.72) for esophageal adenocarci

116 Rab25 may provide a prognostic biomarker for ESCC outcome prediction and a novel therapeutic target i

117 ion was an independent prognostic factor for ESCC survival (P = 0.03).

118 could be a clinically applicable marker for ESCC progression.

119 , current smokers were at increased risk for ESCC (hazard ratio (HR) = 9.27, 95% confidence interval

120 1, did not significantly modify the risk for ESCC or EAC in our Dutch population.

121 tin-expressing distal esophageal/forestomach ESCC.

122 Human ESCC cell lines, TE-11 with high and TT with minimal per

123 DNA was extracted from 16 human ESCC cell lines and microdissected tumor specimens from

124 grown in three-dimensional culture and human ESCC revealed identical features, including significantl

125 lations and fast cell proliferation in human ESCC cells.

126 EGFR overexpression are able to mimic human ESCC in a relevant three-dimensional culture model.

127 DAR2B was methylated in 95% of primary human ESCC tissue specimens and 12 ESCC cell lines by sequence

128 op squamous cell cancers that resemble human ESCC, we visualized the probe in preneoplastic and neopl

129 fection, and ESCCs expressing specific human ESCC markers.

130 Here we show that the human ESCC miRNA orthologs hsa-miR-302b and hsa-miR-372 promot

131 mor-invasive signature classifies with human ESCC microarrays, underscoring its utility in human canc

132 In ESCC xenograft tumours, pharmacological autophagy inhibi

133 shortening is a common genetic alteration in ESCC and that chromosome arm instability is related to b

134 ed by marked Ca(2+)-independent apoptosis in ESCC cell lines, suggesting that NMDAR2B can suppress tu

135 es) and Human U133A (n = 17 cases) arrays in ESCC cases from a high-risk region of China.

136 conclude that germline mutations in BRCA2 in ESCC patients from this high-risk area of China are more

137 NPs were associated with FH of UGI cancer in ESCC cases with P < 10(-5) in the stage-1 meta-analysis

138 s, NMDAR2B promoter methylation is common in ESCC, abrogating gene transcription and leading to cellu

139 cycle and PI3K-AKT pathways seem critical in ESCC.

140 overall survival and was also documented in ESCC cell lines compared with pooled normal tissues.

141 Levels of DNAJB6 were knocked down in ESCC cell lines (KYSE450 and T.Tn), immortalized normal

142 sequently IdoA content, was downregulated in ESCC cells.

143 MT1-MMP induced EMT in ESCC both in vivo and in vitro, N-cadherin and Vimentin

144 induced inflammation as a critical factor in ESCC development has important clinical implications wit

145 Here, we report somatic mutations found in ESCC from sequencing 10 whole-genome and 57 whole-exome

146 We therefore examined p16 function in ESCC lines and in primary squamous epithelial cells cult

147 plotypes were associated with an increase in ESCC risk.

148 tive T cells and chronic fungal infection in ESCC development remains unclear.

149 The causes of inflammation in ESCC, however, are undefined.

150 from MS/MS data with functional insights in ESCC.

151 MT led to increase migration and invasion in ESCC cell lines.

152 eby, novel STAT3-regulated genes involved in ESCC and BAC cell proliferation and cell migration were

153 unmasks a number of novel genetic lesions in ESCC and provides an important molecular foundation for

154 s cell motility and lymph node metastasis in ESCC patients, leading to poorer survival.

155 ed a possible role for gastric microbiota in ESCC carcinogenesis.

156 pare pattern of gastric corpus microbiota in ESCC with normal esophagus.

157 ed how the hypoxic tumor microenvironment in ESCC fosters the induction of IGFBP3.

158 ive frequency of BRCA2 germline mutations in ESCC patients in this and our previous study combined is

159 p53(R175H), two common genetic mutations in ESCC.

160 present in both the cytoplasm and nucleus in ESCC cells.

161 the most commonly overexpressed oncogene in ESCC.

162 ion correlates with poor clinical outcome in ESCC.

163 pCR, and FAM84B protein is overexpressed in ESCC.

164 underscore the importance of this pathway in ESCC invasion and progression.

165 imaging of extracellular matrix periostin in ESCC is feasible using a targeted PET tracer.

166 standing of tumorigenesis and progression in ESCC.

167 TAT3 knockdown reduces cell proliferation in ESCC and BAC cells, inhibits migration of BAC cells and

168 ysis suggested their functional relevance in ESCC.

169 herapeutic targeting of HGF/Met signaling in ESCC and potentially other squamous cancers where this p

170 nd identified new candidate loci to study in ESCC.

171 prediction and a novel therapeutic target in ESCC treatment.

172 activation of TCF-dependent transcription in ESCC.

173 tures (E1-E6), and Signature E4 is unique in ESCC linked to alcohol intake and genetic variants in al

174 ulfotransferases, were highly upregulated in ESCC biopsies.

175 tterns of STAT3 expression and activation in ESCCs and BACs.

176 g GASC1, shown previously to be amplified in ESCCs, and EPHB1 and PIK3C3.

177 , n=61) revealed similar STAT3 expression in ESCCs and BACs (P=0.109), but preferentially activated P

178 ly universal inactivation of this pathway in ESCCs.

179 09), but preferentially activated P-STAT3 in ESCCs (P=0.013).

180 otential biomarker and therapeutic target in ESCCs with lymph node metastases.

181 een implicated in several cancers, including ESCC.

182 CD44H cells have been implicated, including ESCC.

183 one-to-three risk genotypes had an increased ESCC risk.

184 1 risk genotypes had significantly increased ESCC risk, particularly for males, ever-smokers, ever-dr

185 Using an independent ESCC cohort, we confirmed that 8/10 of CpG loci in the p

186 chemistry and tissue microarray in 88 Kazakh ESCC patients.

187 xpression of MT1-MMP was confirmed in Kazakh ESCC patients.

188 Treatment of KYSE220 ESCC and BIC EAC cells with 5-aza-2'-deoxycytidine reduc

189 when cultured with Wnt-1-conditioned media, ESCC cell lines showed an accumulation of beta-catenin i

190 In genetically engineered mouse models, ESCC high periostin tracer uptake anatomically correlate

191 Our joint analysis identifies new ESCC susceptibility loci overall as well as a new locus

192 regulation of HMGB1 and calreticulin in nine ESCC cell lines.

193 mal growth factor (EGF) stimulation in OE21 (ESCC) cells, whereas OE33 (BAC) cells showed constitutiv

194 p120ctn is down-regulated in 60% of ESCC tumors, whereas EGFR is the most commonly overexpre

195 and suppressed the proliferation ability of ESCC cells in three-dimensional culture systems and angi

196 itical in modulating the invasive ability of ESCC in an in vivo-like organotypic 3D cell culture, a f

197 HMVEC network formation, and the addition of ESCC cells to these cultures greatly enhanced the angiog

198 een 1995/1996 and 2000, 97 incident cases of ESCC, 205 of esophageal adenocarcinoma, 188 of gastric c

199 odel was used to estimate HRs and 95% CIs of ESCC for dietary intakes of selected minerals.

200 ovel assay was developed where cocultures of ESCC and esophageal fibroblasts induced human microvascu

201 frequent event in a second larger cohort of ESCC tumor specimens by quantitative real-time PCR and i

202 er validated with two independent cohorts of ESCC samples.

203 the role of MT1-MMP in the dissemination of ESCC.

204 erhaps contributing to the high incidence of ESCC in southern South America.

205 (NMBA) elicited a 66.7% (16/24) incidence of ESCC.

206 tablish a comprehensive genomic landscape of ESCC and provide potential targets for precision treatme

207 genesis underlying the invasive mechanism of ESCC is not well known because of the lack of existing m

208 reveal periostin as an important mediator of ESCC tumor invasion and they indicate that organotypic (

209 s well as popliteal lymph node metastases of ESCC cells in nude mice (P = 0.020).

210 BAC cells and may support cell migration of ESCC cells.

211 pressor gene involved in the pathogenesis of ESCC.

212 contribute to the molecular pathogenesis of ESCC.

213 rentially methylated CpG sites prognostic of ESCC progression.

214 developed as a biomarker for progression of ESCC.

215 tion significantly inhibits proliferation of ESCC cell lines and that the effect of zinc is reversibl

216 cantly inversely associated with the risk of ESCC (HR per 100-mg/d increase: 0.88; 95% CI: 0.81, 0.96

217 395 genotype was subtly decrease the risk of ESCC (T vs. C: OR = 0.95; 95%CI = 0.90-0.99; P = 0.02) a

218 and zinc are associated with a lower risk of ESCC in a high-risk region of Iran.

219 -nitroso compounds may influence the risk of ESCC in men, but there are no clear associations for oth

220 selenium, magnesium, and copper and risk of ESCC were nonlinear (P-nonlinear trend = 0.001, 0.016, a

221 iation between physical activity and risk of ESCC with conflicting results, and the meta-analysis dem

222 the Taihang Mountain region at high risk of ESCC.

223 c (Zn)-deficiency (ZD) increases the risk of ESCC.

224 nd impairment of ALDH2 increases the risk of ESCC.

225 dietary intake of manganese and the risk of ESCC.

226 monas gingivalis trended with higher risk of ESCC.

227 ession of DNAJB6a reduced the sensitivity of ESCC to AKT inhibitors; the expression level of DNAJB6a

228 both the dysplastic and neoplastic stages of ESCC development, and prevented cancer formation.

229 vide a promising target for the treatment of ESCC.

230 otypes and smoking (Pinteraction = 0.026) on ESCC risk.

231 n between p120ctn and EGFR and its effect on ESCC invasion.

232 ity in Caucasians, in contrast to results on ESCC from Asia or Africa.

233 ypes in GST genes are not involved in EAC or ESCC susceptibility in Caucasians, in contrast to result

234 Genotypes with similar risks for EAC or ESCC were combined and analyzed for multiplicative effec

235 s were compared between patients with EAC or ESCC, and controls.

236 ated with overall esophageal cancer, EAC, or ESCC risk, although total flavonoids and some flavonoid

237 noid subclass and esophageal cancer, EAC, or ESCC.

238 me or targeted deep sequencing of 139 paired ESCC cases, and analysis of somatic copy number variatio

239 stochemical studies performed on 113 primary ESCC specimens revealed a high prevalence of PTTG1 overe

240 Almost all primary ESCC tissues (95%) showed reduced expression, and 9 of 1

241 In primary ESCC samples, patients whose tumors had high nuclear lev

242 rmed immunohistochemical analyses of primary ESCC samples and lymph node metastases from a cohort of

243 We here report a rare case of primary ESCC with completely intramural growth under a normal lo

244 an exceedingly rare presentation of primary ESCC with only four cases reported in the literature so

245 promoter hypermethylation in 50% of primary ESCCs by methylation-specific PCR.

246 inflammation and epithelial injury, promote ESCC development.

247 n, our results suggest that MT1-MMP promotes ESCC invasion and metastasis.

248 whereas oral fungal administration promotes, ESCC development.

249 Introduction of ESC cell cycle regulating (ESCC) miRNAs into the Dgcr8(-/-) ESCs blocks the capacit

250 ic stem cell-specific cell cycle-regulating (ESCC) family of microRNAs (miRNAs) enhances reprogrammin

251 od at this level of histological resolution, ESCC contains little regional mRNA heterogeneity.

252 In clinical samples, ESCC patients with high expression of CXCR7 and IL6 pres

253 The vertebrate-specific ESCC microRNA family arises from two genetic loci in mam

254 analysis by body mass index (BMI) found that ESCC risk was significantly associated with each of thre

255 Finally, we showed that ESCC-derived TGF-beta regulates angiogenesis through the

256 Together, these findings show how the ESCC and let-7 miRNAs act through common pathways to alt

257 ows the essential role of fibroblasts in the ESCC angiogenic-induced response and suggests that the p

258 on intracellular Ca(2+) oscillations in the ESCC cells.

259 ations in the RNF6 gene were detected in the ESCC primary tumors, and one mutation was also found in

260 d the role of the stromal fibroblasts in the ESCC-induced angiogenic response using a novel 3-dimensi

261 All of the ESCC cores and 96.2% of adenocarcinoma stained positive

262 These results demonstrate that the ESCC miRNAs promote dedifferentiation by acting on multi

263 Biochemical studies showed that the ESCC-induced activation of the fibroblasts was required

264 ificantly reduced cell motility in all three ESCC cell lines (P < 0.01) in vitro, as well as poplitea

265 d PTTG1 mRNA and protein expression in three ESCC cell lines by 77% to 97%.

266 hemoradiation provides a survival benefit to ESCC patients, especially those with pT3/4 stage, N+ tum

267 y functional SNPs in ERCC2 may contribute to ESCC risk.

268 ations and genomic events that contribute to ESCC tumorigenesis and prognosis and might suggest thera

269 cognizes periostin and binds specifically to ESCC xenograft tumors in mice.

270 a promising therapeutic target for treating ESCC.

271 We present a new analysis framework, using ESCC progression-associated gene regulatory network (GRN

272 ic analyses show that let-7 inhibits whereas ESCC miRNAs indirectly activate numerous self-renewal ge

273 tric junctional adenocarcinoma, and 332 with ESCC were matched to 2167, 783, and 1242 controls, respe

274 for 1-4 years was inversely associated with ESCC (odds ratio = 0.51; 95% confidence interval: 0.27-0

275 nc intake was also inversely associated with ESCC, but the quartile association did not reach signifi

276 We observed no association with ESCC risk for any of the selected SNPs.

277 T > G) and assessed their associations with ESCC risk.

278 e controls to assess their associations with ESCC risk.

279 intestinal cancer (UGI) cancer in cases with ESCC.

280 expression profiles of 321 individuals with ESCC indicated that these genes were significantly assoc

281 f DNA and RNA in 94 Chinese individuals with ESCC.

282 e confirmed in six (38%) of 16 patients with ESCC after chemoradiotherapy coexisting with elevated se

283 Patients with ESCC completing CRT followed by surgery were enrolled fo

284 s significantly upregulated in patients with ESCC with preoperative chemoradiotherapy, but not in tho

285 327 patients with EAC and 106 patients with ESCC.

286 with longer survival times of patients with ESCC.

287 Fungal infection is highly associated with ESCCs in non-autoimmune human patients.