ライフサイエンスコーパス: esophageal tumor

1 RHBDF2 in both tylotic and sporadic squamous esophageal tumors.

2 er of gastric, gastroesophageal junction and esophageal tumors.

3 idence of N-nitrosomethylbenzylamine-induced esophageal tumors.

4 r, was overexpressed in all of the amplified esophageal tumors.

5 s was significantly increased, especially in esophageal tumors.

6 SB) gene was found to be amplified in 13% of esophageal tumors.

7 lin D1/Cdk4-Rb pathway and the initiation of esophageal tumors.

8 cers but may be rare in unstable gastric and esophageal tumors.

9 were identified: (a) in one gastric and one esophageal tumor, an A to C transversion occurred at nuc

10 One of 13 primary esophageal tumors analysed by RT-PCR expressed no detect

11 rated progression to malignancy, with 10% of esophageal tumors and 38% of forestomach tumors presenti

12 rtant molecular foundation for understanding esophageal tumors and developing therapeutic targets.

13 Additionally, 14% of ZD:TG mice developed esophageal tumors and esophageal intestinal metaplasia a

14 t, lung, pancreatic, ovarian, head/neck, and esophageal tumors and found that 69% of all specimens st

15 squamous cell cancer, 6 had another form of esophageal tumor, and 6 had high-grade dysplasia associa

16 frequency of 14q13 amplification is 6.7% in esophageal tumors, and the amplicon spans >6 Mb in 1 tum

17 cells that have been implicated in oral and esophageal tumor biology.

18 rmal mucosae, 30 dysplastic lesions, and 157 esophageal tumors by in situ hybridization.

19 l squamous cell transformation, we generated esophageal tumor cells using human telomerase- and SV40-

20 lysis revealed that none of these 11 primary esophageal tumors contained any alterations in the FHIT

21 mmune checkpoint modification contributes to esophageal tumor development.

22 ons can be seen in the premalignant stage of esophageal tumor development.

23 r NMBA dosing, DFMO reduced the incidence of esophageal tumors from 80 to 4% in zinc-deficient rats.

24 ogression was supported by data showing that esophageal tumors from human patients show reduced CcO s

25 ration, migration, and invasion in vitro and esophageal tumor growth in vivo.

26 >Pro substitution at codon 179; (b) a second esophageal tumor had a C to T transition at nucleotide 8

27 d squamous epithelia and the absence of oral-esophageal tumors in p53-null mice, we postulated and de

28 NOS inhibitor, to prevent the progression of esophageal tumors in rats preinitiated with NMBA.

29 geal cell proliferation and the induction of esophageal tumors in rodents by N-nitrosomethylbenzylami

30 After 14 weeks, esophageal tumor incidence was 88% in ZD rats with highl

31 e diet produced no significant reductions in esophageal tumor incidence, multiplicity, or size.

32 Amplified genes were noted in 37% of gastric/esophageal tumors, including in therapeutically targetab

33 zinc deficiency and reduced the incidence of esophageal tumors induced by a single dose of NMBA in zi

34 uced apoptosis under conditions that reverse esophageal tumor initiation.

35 R1 resection margin included an upper third esophageal tumor location, preoperative malnutrition, an

36 he esophagus, there is an increased yield of esophageal tumors, many of which are adenocarcinomas.

37 Based on current guidelines, clinical T3N0M0 esophageal tumors may or may not receive neoadjuvant tre

38 Periostin might be a biomarker of the esophageal tumor microenvironment that can be used to de

39 We investigated a total of 63 primary esophageal tumors, nine esophageal cancer cell lines and

40 tive inhibitor, PBIT, significantly inhibits esophageal tumor progression presumably through reducing

41 In an additional 50 esophageal tumors, the polymorphic microsatellite loci D

42 r types of esophagitis, benign and malignant esophageal tumors, varices, lower esophageal rings, dive

43 developed forestomach tumors and 38% showed esophageal tumors versus 42 and 0% in ZS:p53-/- mice (P

44 2) in non-small cell lung cancer, but in the esophageal tumors, volume and heterogeneity had less com

45 In 13 esophageal tumors, we employed overlapping reverse trans

46 Resected esophageal tumors were assessed for pathologic response

47 t 25 weeks, the animals were sacrificed, and esophageal tumors were counted.

48 cluding a recurrent deletion found in 15% of esophageal tumors where the Runt transcription factor su

49 ma (ESCC) is the commonest primary malignant esophageal tumor, which typically presents as endoscopic

50 dies in 36 patients with stage T2 or greater esophageal tumors who underwent contrast-enhanced CT bef