The spectrum of carcinoma arising in Barrettʼs esophagus

Smith, Robert R.; Hamilton, Stanley R.; Boitnott, J. K.; Rogers, Eammon

doi:10.1097/00000478-198408000-00001

Cited by 172 publications

(56 citation statements)

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“…Unfortunately, the epidemiology of Barrett's esophagus is incompletely described. However, we know from series of surgical resections of adenocarcinoma of the esophagus associated with Barrett's esophagus that, among patients, white men overwhelmingly predominate (3)(4)(5)(6)(7). Additionally, there are data suggesting that the longer the duration of reflux symptoms, the higher the prevalence of Barrett's esophagus at the time of upper endoscopy (19,20).…”

Section: When To Look For Barrett's Esophagus In Patients With Gastromentioning

confidence: 99%

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Sampliner

1998

The American Journal of Gastroenterology

105

110

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Section: When To Look For Barrett's Esophagus In Patients With Gastromentioning

confidence: 99%

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Sampliner

1998

The American Journal of Gastroenterology

105

110

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“…The presence of Barrett's dysplasia, particularly high-grade dysplasia, is one of the risk factors for adenocarcinoma (Reid et al, 1988;Schmidt et al, 1985;Smith et al, 1984). An unsuspected adenocarcinoma is identified in approximately 30-40% of esophagi that are resected for high-grade dysplasia (Falk et al, 1999;Gilbert and Jobe, 2009;Hameeteman et al, 1989;Hamilton and Smith, 1987;Lee, 1985).…”

Section: Introductionmentioning

confidence: 99%

Conversion of metaplastic Barrett’s epithelium into post-mitotic goblet cells by γ-secretase inhibition

Menke¹,

Lau

et al. 2010

Disease Models &Amp; Mechanisms

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SUMMARYBarrett's esophagus (BE) affects approximately 2% of the Western population and progresses to esophageal adenocarcinoma (EAC) in 0.5% of these patients each year. In BE, the stratified epithelium is replaced by an intestinal-type epithelium owing to chronic gastroduodenal reflux. Since selfrenewal of intestinal crypts is driven by Notch signaling, we investigated whether this pathway was active in the proliferative crypts of BE. Immunohistochemistry confirmed the presence of an intact and activated Notch signaling pathway in metaplastic BE epithelium, but not in the normal human esophagus. Similar observations were made in two well-known human Barrett's-derived EAC cell lines, OE33 and SKGT-5. We then sought to investigate the effects of Notch inhibition by systemic treatment with a -secretase inhibitor in a well-validated rodent model for BE. As we have shown previously in normal intestinal epithelium, Notch inhibition converted the proliferative Barrett's epithelial cells into terminally differentiated goblet cells, whereas the squamous epithelium remained intact. These data imply that local application of -secretase inhibitors may present a simple therapeutic strategy for this increasingly common pre-malignant condition.

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“…[1][2][3] It is characterized by a columnar change in the distal esophageal squamous epithelium that can be recognized at endoscopy, and is confirmed to have intestinal (specialized) metaplasia by biopsy. 4 Although the specialized columnar epithelium is composed of both goblet and columnar non goblet cells, only the former are considered as the hallmark of Barrett's esophagus.…”

mentioning

confidence: 99%

Expression of the intestinal marker Cdx2 in the columnar-lined esophagus with and without intestinal (Barrett's) metaplasia

2004

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Barrett's esophagus is diagnosed when goblet cells are found in the lower esophageal mucosa. However, the distribution of these cells is patchy and they may not represent the earliest marker of intestinal metaplasia. Cdx2 is a transcription factor whose expression in normal tissues is restricted to intestinal-type epithelium. Its distribution in the columnar-lined esophagus with and without intestinal metaplasia has been seldom studied. We evaluated Cdx2 expression in lower esophageal biopsies from 90 patients with endoscopic diagnosis of short segment Barrett's esophagus, including 45 consecutive cases showing intestinal metaplasia (goblet cells present in hematoxylin eosin and/or Alcian blue stains) and 45 consecutive cases without goblet cells. 25 samples of cardiac-type mucosa without intestinal metaplasia biopsied from the stomach served as controls. All cases with intestinal metaplasia revealed Cdx2 reactivity in goblet cells and adjacent nongoblet columnar cells. Dysplastic foci, seen in five cases from this group, were Cdx2 positive. In the group without goblet cells, Cdx2 was focally expressed by columnar cells in 17 (38%) cases. All control cases were Cdx2 negative. Strips of Alcian blue-positive nongoblet columnar cells ('columnar blues') were observed in 11 (24%) of the cases without intestinal metaplasia. All these foci were Cdx2 negative. In conclusion, Cdx2 is a highly sensitive marker for Barrett's esophagus. It is also expressed in a significant minority of cases of columnar-lined esophagus without goblet cells, suggesting that it may detect intestinal phenotypic modifications in the absence of goblet cells. Accordingly, Cdx2 immunostaining could help identify patients with Barrett's metaplasia in cases where no goblet cells are visible in biopsies from the columnar-lined esophagus. Finally, lack of Cdx2 expression in the 'columnar blues' suggests that these cells are not diagnostic of intestinal metaplasia.

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The spectrum of carcinoma arising in Barrettʼs esophagus

Cited by 172 publications

References 0 publications

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Conversion of metaplastic Barrett’s epithelium into post-mitotic goblet cells by γ-secretase inhibition

Expression of the intestinal marker Cdx2 in the columnar-lined esophagus with and without intestinal (Barrett's) metaplasia

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