Barrettʼs Esophagus

Skinner, David B.; Walther, Bruno; Riddell, Robert H.; Schmidt, H; Iascone, Clement; Demeester, Thomas

doi:10.1097/00000658-198310000-00016

Cited by 467 publications

(41 citation statements)

References 19 publications

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“…Recent evidence suggests that specialized columnar epithelium containing goblet cells is the metaplastic tissue of importance in Barrett’s esophagus, given that most AEs are associated with this type of epithelium, also referred to as ‘intestinal metaplasia’ [14, 15, 16]. Furthermore, recent Western studies have suggested an association between AEGJ and Barrett’s esophagus [9, 11].…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, it is well established that the majority of AEs arise from intestinal metaplasia of Barrett’s esophagus [14, 15, 16]. In the present study, despite the fact that both EAGC and EAE were associated with a greater incidence of differentiated-type tumors than EADS, the prevalence of intestinal metaplasia (specialized columnar epithelium) in surrounding non-neoplastic mucosa in the patients with EAGC (36.7%, 18/49 patients) was significantly lower than in the patients with EADS or EAE (72.0%, 211/293, and 85.7%, 6/7).…”

Section: Discussionmentioning

confidence: 99%

“…These findings suggest an association between AEGJ and Barrett’s esophagus. This may at least in part explain the relationship between AEGJ and Barrett’s esophagus, since there is a well-established association between AE and intestinal metaplasia in Barrett’s esophagus [12, 13, 14, 15, 16]. However, it is difficult to discuss the association between AEGJ and Barrett’s esophagus or intestinal metaplasia of the gastric cardia on the basis of previous studies, because the tumors analyzed had for the most part reached the advanced stage and they were large.…”

Section: Introductionmentioning

confidence: 99%

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Clinicopathological Study of Early Adenocarcinoma of the Gastric Cardia: Comparison with Early Adenocarcinoma of the Distal Stomach and Esophagus

Tajima

Nakanishi²,

Yoshino³

et al. 2001

Oncology

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To clarify the clinicopathological characteristics of adenocarcinoma of the gastric cardia (AGC), including its association with Barrett’s esophagus and intestinal metaplasia, 49 surgically resected early AGCs (EAGCs) were examined clinicopathologically, histopathologically, histochemically, and immunohistochemically. The clinicopathological characteristics of the patients with EAGC were compared with those of 293 patients with early adenocarcinoma of the distal stomach (EADS) and 7 patients with early adenocarcinoma of the esophagus (EAE). Histochemical staining with paradoxical concanavalin A (ConA) and immunohistochemical staining with monoclonal antibodies 45M1, Ccp58, and 56C6 were performed to investigate the differentiation phenotype of the tumor. ConA and 45M1 were used for markers of the gastric phenotype, and Ccp58 and 56C6 were used for markers of the intestinal phenotype. EAGC was associated with a higher mean age (p < 0.0001), a higher male-to-female ratio (p < 0.05), a higher incidence of elevated-type tumors (p < 0.0001), a higher incidence of differentiated-type tumors (p < 0.0001), and greater depth of invasion (p < 0.05) compared with EADS. EAE was associated with a higher incidence of elevated-type tumors (p < 0.001), a higher incidence of differentiated-type tumors (p < 0.05), and larger tumor size (p < 0.05) compared with EADS. The prevalence of Barrett’s esophagus in patients with EAGC was significantly lower than in patients with EAE (10.2%, 5/49 patients vs. 100%, 7/7; p < 0.0001). The prevalence of intestinal (Barrett’s) metaplasia in surrounding non-neoplastic mucosa in patients with EAGC was significantly lower than in patients with EADS or EAE (36.7%, 18/49 patients vs. 72.0%, 211/293 and 85.7%, 6/7; p < 0.0001 and p < 0.05, respectively). EAGC was associated with a higher incidence of tumors that reacted positively for gastric phenotype markers alone than EADS (32.7%, 16/49 cases vs. 17.1%, 50/293; p < 0.05) and a lower incidence of tumors that reacted positively for both gastric and intestinal markers than EADS or EAE (40.8%, 20/49 cases vs. 59.7%, 175/293 and 85.7%, 6/7; p < 0.05, respectively). Our findings indicate that AGC forms a specific category different from both adenocarcinoma of the distal stomach and esophagus in terms of association with Barrett’s esophagus or intestinal metaplasia, and the differentiation phenotype of the tumor.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Clinicopathological Study of Early Adenocarcinoma of the Gastric Cardia: Comparison with Early Adenocarcinoma of the Distal Stomach and Esophagus

Tajima

Nakanishi²,

Yoshino³

et al. 2001

Oncology

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“…Barrett's-associated cancers do not arise de novo, but rather evolve from a multi-step process in which the metaplastic columnar epithelium sequentially develops through a dysplasiacarcinoma sequence (Skinner et al, 1983;Hameeteman et al, 1989;Reid, 1991). As BE progresses to dysplasia and adenocarcinoma, increased and uncoordinated cell proliferation and decreased expression of di erentiation markers have been observed (Fitzgerald and Triada®lopoulos, 1998).…”

Section: Introductionmentioning

confidence: 99%

Proton pump inhibitors reduce cell cycle abnormalities in Barrett's esophagus

Umansky

W²,

Hallak

et al. 2001

Oncogene

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Neoplastic progression in Barrett's esophagus is a multistep process in which the metaplastic columnar epithelium sequentially evolves through a metaplasia-dysplasiacarcinoma sequence. The expression and DNA copy number of key cell cycle regulatory genes in paired normal and Barrett's esophagus samples was evaluated. Protein levels were evaluated in 60 formalin-®xed, para n-embedded human tissues by immunohistochemistry. DNA copy number from 20 fresh tissue pairs was analysed by Southern blot analysis. All normal mucosal samples expressed the p27 kip1 protein, but did not display appreciable nuclear staining for p16 kip4 , p21 cip1 or cyclins D1 and E. Barrett's metaplastic specimens displayed increased expression levels of p16 kip4 (74%), p21 cip1 (89%) and cyclins D1 (43%) and E (37%). p27 protein was absent in three cases. There was a signi®cant correlation between the expression of p16 kip4 and cyclin E, and p21 cip1 and p27 kip4 with cyclin D1. DNA analysis did not reveal any ampli®cation or deletion of these genes. Acid suppression, however, was associated with signi®cantly lower expression levels of key cell cycle proteins. Increased expression of key cell cycle regulatory genes appears to occur early in the neoplastic progression associated with Barrett's esophagus. Treatment with proton pump inhibitors appears to alter this increased expression. Oncogene (2001) 20, 7987 ± 7991.

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“…People from the Western hemisphere tend to develop esophageal cancer from prior metaplastic mucosal transformation referred to as Barrett's esophagus (BE) [2]. BE is fre- …”

Section: Introductionmentioning

confidence: 99%

Diffuse reflectance spectroscopy in Barrett’s Esophagus: developing a large field‐of‐view screening method discriminating dysplasia from metaplasia

Douplik

Zanati

Saiko

et al. 2012

Journal of Biophotonics

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We evaluated diffuse reflectance spectroscopy implemented as a small field‐of‐view technique for discrimination of dysplasia from metaplasia in Barrett’s esophagus as an adjuvant to autofluorescence endoscopy. Using linear discriminant analysis on 2579 spectra measured in 54 patients identified an optimum a 4‐wavelength classifier (at 485, 513, 598 and 629 nm). Sensitivity and specificity for a test data set were 0.67 and 0.85, respectively. Spectroscopic results show that this technique could be implemented in wide‐field imaging mode to improve the accuracy of existing endoscopy techniques for finding early pre‐malignant lesions in Barrett’s esophagus. Results show that the discrimination occurs likely due to redistribution of blood content in the tissue sensed by the optical probing with the wavelength‐dependent sampling depth. (© 2014 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)

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Barrettʼs Esophagus

Cited by 467 publications

References 19 publications

Clinicopathological Study of Early Adenocarcinoma of the Gastric Cardia: Comparison with Early Adenocarcinoma of the Distal Stomach and Esophagus

Clinicopathological Study of Early Adenocarcinoma of the Gastric Cardia: Comparison with Early Adenocarcinoma of the Distal Stomach and Esophagus

Proton pump inhibitors reduce cell cycle abnormalities in Barrett's esophagus

Diffuse reflectance spectroscopy in Barrett’s Esophagus: developing a large field‐of‐view screening method discriminating dysplasia from metaplasia

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