ライフサイエンスコーパス: ESCC

1 ESCC classically progresses rapidly and frequently cause

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

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

4 ESCC-free, Zn-deficient miR-31(-/-) rat esophagus displa

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

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

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

8 Nuclear YAP expression was elevated in 197 ESCC tissues from a Chinese cohort.

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

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

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

12 rs, normal tissues and blood samples from 39 ESCC patients.

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

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

15 37 ESCC cases and 5,787 controls) with 9,654 ESCC cases and 10,058 controls for follow-up.

16 study of 184 patients with locally advanced ESCC.

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

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

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

20 ges vs. the pronounced mutational burden and ESCC-associated metabolic changes of Zn-deficient wild-t

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

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

23 h normal differentiated esophageal cells and ESCC, respectively.

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

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

26 he early detection and prevention of EAC and ESCC.

27 association between different exposures and ESCC.

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

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

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

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

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

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

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

35 We also associated ESCC risk with exposure to unpiped water and tooth loss.

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

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

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

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

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

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

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

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

44 atlas of esophageal squamous cell carcinoma (ESCC) at single-cell resolution.

45 000 new oesophageal squamous-cell carcinoma (ESCC) cases each year occur in China.

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

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

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

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

50 ctor for esophageal squamous cell carcinoma (ESCC) have been inconsistent.

51 rkers in esophageal squamous cell carcinoma (ESCC) have not been widely explored.

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

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

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

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

56 Esophageal squamous cell carcinoma (ESCC) is among the most aggressive and fatal cancer type

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

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

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

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

61 eficient esophageal squamous cell carcinoma (ESCC) models, reciprocal to the known synthetic lethal i

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

63 Esophageal squamous cell carcinoma (ESCC) ranks fourth among cancer-related deaths in China

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

65 f YAP in esophageal squamous cell carcinoma (ESCC) remains unclear.

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

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

68 nts with esophageal squamous cell carcinoma (ESCC) who do not benefit from standard chemoradiation (C

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

70 rates of esophageal squamous cell carcinoma (ESCC) worldwide.

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

72 essed in esophageal squamous cell carcinoma (ESCC), a deadly disease associated with dietary Zn defic

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

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

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

76 176 were esophageal squamous cell carcinoma (ESCC), and 23 were other types of esophageal cancer.

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

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

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

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

81 uency in esophageal squamous cell carcinoma (ESCC), where it promotes ESCC development and progressio

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

83 nesis of esophageal squamous cell carcinoma (ESCC).

84 tion and esophageal squamous cell carcinoma (ESCC).

85 pCR for esophageal squamous cell carcinoma (ESCC).

86 causes oesophageal squamous cell carcinoma (ESCC).

87 nesis of esophageal squamous cell carcinoma (ESCC).

88 risk of esophageal squamous cell carcinoma (ESCC).

89 odels of esophageal squamous cell carcinoma (ESCC).

90 ivers of esophageal squamous cell carcinoma (ESCC).

91 risk of esophageal squamous cell carcinoma (ESCC).

92 loci for esophageal squamous cell carcinoma (ESCC).

93 risk of esophageal squamous cell carcinoma (ESCC).

94 nesis of esophageal squamous cell carcinoma (ESCC).

95 nts with esophageal squamous cell carcinoma (ESCC).

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

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

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

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

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

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

102 ressing esophageal squamous cell carcinomas (ESCCs).

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

104 ars of follow-up, 317 participants developed ESCC.

105 stepwise increase in the risk of developing ESCC, reaching a more than 7-fold increase in risk in th

106 fector molecules can efficiently distinguish ESCC patients into low- and high-risk groups.

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

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

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

110 get in esophageal cancer using an engineered ESCC cell model harboring a SMARCA4 allele amenable to t

111 m an organotypic culture model of engineered ESCC.

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

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

114 tric atrophy appears to be a risk factor for ESCC in a high-risk region of China, and there is a sugg

115 in Iran identified multiple risk factors for ESCC in this population.

116 ence that miR-31 expression is necessary for ESCC development.

117 L) was associated with an increased risk for ESCC (odds ratio = 1.61; 95% confidence interval: 1.33,

118 1, did not significantly modify the risk for ESCC or EAC in our Dutch population.

119 d provide a promising therapeutic target for ESCC treatment in the clinic.

120 tin-expressing distal esophageal/forestomach ESCC.

121 , cancer-associated inflammation, and a high ESCC burden following N-nitrosomethylbenzylamine (NMBA)

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

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

124 lations and fast cell proliferation in human ESCC cells.

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

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

127 fection, and ESCCs expressing specific human ESCC markers.

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

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

130 nd inflammation was also documented in human ESCCs.

131 In ESCC xenograft tumours, pharmacological autophagy inhibi

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

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

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

135 ically increased sensitivity to cisplatin in ESCC cells.

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

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

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

139 sequently IdoA content, was downregulated in ESCC cells.

140 is combined treatment has potent efficacy in ESCC cells with acquired resistance to CDK4/6 inhibitors

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

142 te tumor growth and CSC marker expression in ESCC xenografts.

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

144 edback loop and confers CSC-like features in ESCC, suggesting that this YAP-SOX9 circuit represents a

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

146 pe; as such, these findings are important in ESCC as well as in other cancer types.

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 ew AURKA-SDCBP-EGFR axis that is involved in ESCC progression and provide a promising therapeutic tar

154 Collectively, we reveal high-level ITH in ESCC, identify several potential actionable targets and

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

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

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

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

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

160 vity associated with actionable mutations in ESCC.

161 the most commonly overexpressed oncogene in ESCC.

162 ion correlates with poor clinical outcome in ESCC.

163 rt that SDCBP is frequently overexpressed in ESCC tissues and cells compared to normal controls and t

164 pCR, and FAM84B protein is overexpressed in ESCC.

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

166 fferentially expressed genes and pathways in ESCC by bioinformatics analysis, potentially providing v

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

168 linical stage and predicts poor prognosis in ESCC patients.

169 two genes associated with poor prognosis in ESCC, work together to cause invasion.

170 standing of tumorigenesis and progression in ESCC.

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

172 ysis suggested their functional relevance in ESCC.

173 taminolysis and mitochondrial respiration in ESCC with dysregulated Fbxo4-cyclin D1 axis as well as c

174 ay reactivate anti-tumor immune responses in ESCC.

175 d underlying molecular mechanism of SDCBP in ESCC remain obscure.

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

177 prediction and a novel therapeutic target in ESCC treatment.

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

179 ulfotransferases, were highly upregulated in ESCC biopsies.

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

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

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

183 een implicated in several cancers, including ESCC.

184 CD44H cells have been implicated, including ESCC.

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

186 1 risk genotypes had significantly increased ESCC risk, particularly for males, ever-smokers, ever-dr

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

188 e targets and may provide novel insight into ESCC treatment.

189 chemistry and tissue microarray in 88 Kazakh ESCC patients.

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

191 ttle is known about the mechanisms that make ESCC so aggressive.

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

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

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

195 Notably, ESCC samples from The Cancer Genome Atlas (TCGA) dataset

196 e uncovered and validated as potential novel ESCC driver alterations.

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

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

199 ation, invasion, and metastasis abilities of ESCC cells via transforming growth factor-beta (TGFbeta)

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

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

202 ficient rats revealed the molecular basis of ESCC abrogation by miR-31 knockout.

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

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

205 er validated with two independent cohorts of ESCC samples.

206 iR-31 gene knockout abrogated development of ESCC (P = 1 x 10(-6)).

207 shed a light for screening and diagnosis of ESCC in future.

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

209 s of the major environmental risk factors of ESCC.

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

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

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

213 e novel insights into clinical management of ESCC.

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

215 information for the molecular mechanisms of ESCC.

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

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

218 rentially methylated CpG sites prognostic of ESCC progression.

219 mechanisms driving aggressive progression of ESCC by P. gingivalis.

220 developed as a biomarker for progression of ESCC.

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

222 upport the hypothesis that the high rates of ESCC are due to a combination of factors, including ther

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

224 395 genotype was subtly decrease the risk of ESCC (T vs. C: OR = 0.95; 95%CI = 0.90-0.99; P = 0.02) a

225 n with poor oral health elevated the risk of ESCC in a high-risk region of China.

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

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

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

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

230 nificantly associated with increased risk of ESCC, in a dose-dependent manner.

231 nd impairment of ALDH2 increases the risk of ESCC.

232 dietary intake of manganese and the risk of ESCC.

233 the Taihang Mountain region at high risk of ESCC.

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

235 monas gingivalis trended with higher risk of ESCC.

236 ergy production and increased sensitivity of ESCC cells to combined treatment with CB-839 (glutaminas

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

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

239 valis is associated with shorter survival of ESCC patients.

240 vide a promising target for the treatment of ESCC.

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

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

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

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

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

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

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

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

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

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

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

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

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

254 inflammation and epithelial injury, promote ESCC development.

255 URKA prevents SDCBP degradation and promotes ESCC tumor growth through the EGFR-PI3K-Akt signaling pa

256 ous cell carcinoma (ESCC), where it promotes ESCC development and progression.

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

258 whereas oral fungal administration promotes, ESCC development.

259 In a Zn deficiency-promoted rat ESCC model with miR-31 up-regulation, cancer-associated

260 posure, systemic antimiR-31 delivery reduced ESCC incidence from 85 to 45% (P = 0.038) and miR-31 gen

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

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

263 A4, while engineered loss of SMARCA2 renders ESCC models vulnerable to concomitant depletion of SMARC

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

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

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

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

268 nd 98% of CpGs are hypomethylated across the ESCC genome.

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

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

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

272 Approximately 75% of the ESCC cases in this region can be attributed to a combina

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

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

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

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

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

278 expression of SDCBP is positively related to ESCC progression both in vitro and in vivo.

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

280 a promising therapeutic target for treating ESCC.

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

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

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

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

285 expressed genes and pathways associated with ESCC by comprehensive bioinformatics analysis.

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

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

288 e controls to assess their associations with ESCC risk.

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

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

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

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

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

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

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

296 with longer survival times of patients with ESCC.

297 327 patients with EAC and 106 patients with ESCC.

298 actionable mutations from 161 patients with ESCC.

299 cessfully established from 123 patients with ESCC.

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