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1 ication and analysis of ctDNA from localized esophageal tumors.
2 RHBDF2 in both tylotic and sporadic squamous esophageal tumors.
3 er of gastric, gastroesophageal junction and esophageal tumors.
4 idence of N-nitrosomethylbenzylamine-induced esophageal tumors.
5 r, was overexpressed in all of the amplified esophageal tumors.
6 s was significantly increased, especially in esophageal tumors.
7 SB) gene was found to be amplified in 13% of esophageal tumors.
8 lin D1/Cdk4-Rb pathway and the initiation of esophageal tumors.
9 cers but may be rare in unstable gastric and esophageal tumors.
10  were identified: (a) in one gastric and one esophageal tumor, an A to C transversion occurred at nuc
11                            One of 13 primary esophageal tumors analysed by RT-PCR expressed no detect
12 whole-genome bisulfite sequencing data on 45 esophageal tumor and nonmalignant samples from both subt
13 rated progression to malignancy, with 10% of esophageal tumors and 38% of forestomach tumors presenti
14 rtant molecular foundation for understanding esophageal tumors and developing therapeutic targets.
15    Additionally, 14% of ZD:TG mice developed esophageal tumors and esophageal intestinal metaplasia a
16 t, lung, pancreatic, ovarian, head/neck, and esophageal tumors and found that 69% of all specimens st
17  squamous cell cancer, 6 had another form of esophageal tumor, and 6 had high-grade dysplasia associa
18  frequency of 14q13 amplification is 6.7% in esophageal tumors, and the amplicon spans >6 Mb in 1 tum
19  cells that have been implicated in oral and esophageal tumor biology.
20 er, as well as DNA from leukocytes and fixed esophageal tumor biopsy samples collected during esophag
21 , tracheoesophageal fistula in patients with esophageal tumors, bronchial perforation and esophagores
22 rmal mucosae, 30 dysplastic lesions, and 157 esophageal tumors by in situ hybridization.
23 l squamous cell transformation, we generated esophageal tumor cells using human telomerase- and SV40-
24 lysis revealed that none of these 11 primary esophageal tumors contained any alterations in the FHIT
25 mmune checkpoint modification contributes to esophageal tumor development.
26 ons can be seen in the premalignant stage of esophageal tumor development.
27 to localize those PET/CT and CT undetectable esophageal tumors for radiotherapy planning.
28 r NMBA dosing, DFMO reduced the incidence of esophageal tumors from 80 to 4% in zinc-deficient rats.
29 ogression was supported by data showing that esophageal tumors from human patients show reduced CcO s
30 ration, migration, and invasion in vitro and esophageal tumor growth in vivo.
31 >Pro substitution at codon 179; (b) a second esophageal tumor had a C to T transition at nucleotide 8
32 d squamous epithelia and the absence of oral-esophageal tumors in p53-null mice, we postulated and de
33 NOS inhibitor, to prevent the progression of esophageal tumors in rats preinitiated with NMBA.
34 geal cell proliferation and the induction of esophageal tumors in rodents by N-nitrosomethylbenzylami
35                              After 14 weeks, esophageal tumor incidence was 88% in ZD rats with highl
36 e diet produced no significant reductions in esophageal tumor incidence, multiplicity, or size.
37 Amplified genes were noted in 37% of gastric/esophageal tumors, including in therapeutically targetab
38 zinc deficiency and reduced the incidence of esophageal tumors induced by a single dose of NMBA in zi
39 uced apoptosis under conditions that reverse esophageal tumor initiation.
40  R1 resection margin included an upper third esophageal tumor location, preoperative malnutrition, an
41 he esophagus, there is an increased yield of esophageal tumors, many of which are adenocarcinomas.
42  distances from the incisors to the proximal esophageal tumor margin were 27.3 +/- 6.4 cm (range 17.1
43 e distance from the incisors to the proximal esophageal tumor margin.
44  distances from the incisors to the proximal esophageal tumor margins were determined by endoscopy an
45 Based on current guidelines, clinical T3N0M0 esophageal tumors may or may not receive neoadjuvant tre
46        Periostin might be a biomarker of the esophageal tumor microenvironment that can be used to de
47        We investigated a total of 63 primary esophageal tumors, nine esophageal cancer cell lines and
48 al cancer cells and single-cell RNA-seq from esophageal tumors of patients unresponsive to RT link ra
49 tive inhibitor, PBIT, significantly inhibits esophageal tumor progression presumably through reducing
50                          In an additional 50 esophageal tumors, the polymorphic microsatellite loci D
51 r types of esophagitis, benign and malignant esophageal tumors, varices, lower esophageal rings, dive
52  developed forestomach tumors and 38% showed esophageal tumors versus 42 and 0% in ZS:p53-/- mice (P
53 2) in non-small cell lung cancer, but in the esophageal tumors, volume and heterogeneity had less com
54                                        In 13 esophageal tumors, we employed overlapping reverse trans
55                                     Resected esophageal tumors were assessed for pathologic response
56 t 25 weeks, the animals were sacrificed, and esophageal tumors were counted.
57 reatment endoscopy and FDG PET/CT detectable esophageal tumors were recruited retrospectively.
58                Thirty-four patients, with 35 esophageal tumors, were included.
59 cluding a recurrent deletion found in 15% of esophageal tumors where the Runt transcription factor su
60 ma (ESCC) is the commonest primary malignant esophageal tumor, which typically presents as endoscopic
61 dies in 36 patients with stage T2 or greater esophageal tumors who underwent contrast-enhanced CT bef