Barrett's Esophagus; Development of Dysplasia and Adenocarcinoma

Hameeteman, W.; Tytgat, G. N. J.; Houthoff, H. J.; Tweel, Jan G. van den

doi:10.1016/s0016-5085(89)80011-3

Cited by 801 publications

(393 citation statements)

References 32 publications

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“…8 Other studies have suggested that the presence of intestinal metaplasia of the esophagus, that is, Barrett esophagus, has a greater impact on prognosis. Barrett esophagus is a preneoplastic precursor lesion of adenocarcinomas of the distal esophagus and esophagogastric junction 9,10 and is found in association with approximately 60% of esophageal adenocarcinomas. 11 Like Barrett esophagus, adenocarcinomas of the esophagus and esophagogastric junction are more frequently found in men over the age of 65 years, many of whom have a history of gastroesophageal reflux disease.…”

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confidence: 99%

The dichotomy in carcinogenesis of the distal esophagus and esophagogastric junction: intestinal-type vs cardiac-type mucosa-associated adenocarcinoma

et al. 2011

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Adenocarcinoma of the distal esophagus and esophagogastric junction continues to rise in incidence. An intestinal metaplasia (Barrett esophagus)-dysplasia-carcinoma sequence induced by gastroesophageal reflux disease is well established. However, a significant number of adenocarcinomas in the vicinity of the esophagogastric junction are seen in the background of gastric/cardiac-type mucosa without intestinal metaplasia. Thus, the aim of this study was to investigate the role of Barrett esophagus (intestinal-type mucosa) in the classification and prognosis of tumors of the distal esophagus and esophagogastric junction. Clinicopathological and molecular characteristics were examined in 157 consecutively resected adenocarcinomas of the distal esophagus and esophagogastric junction and were compared between tumors arising in association with intestinal-type and cardiac-type mucosa. Intestinal-type mucosa-associated adenocarcinomas were more likely to be associated with younger age (P ¼ 0.0057), reflux symptoms (Po0.0001), proximal location (P ¼ 0.0009), lower T stage (Po0.0001), fewer nodal metastases (P ¼ 0.0001), absence of lymphatic (Po0.0001), venous (P ¼ 0.0060) or perineural (Po0.0001) invasion. Histologically, intestinal-type mucosa-associated tumors were more likely to be low-grade glandular tumors (P ¼ 0.0095) of intestinal or mixed immunophenotype (P ¼ 0.015) and express nuclear b-catenin (P ¼ 0.0080), whereas tumors arising in a background of cardiac-type mucosa were more frequently associated with EGFR amplification (P ¼ 0.0051). Five-year overall survival rate was significantly higher in patients with intestinal-type mucosa-associated tumors (28 vs 9%, P ¼ 0.0015), although no survival benefit was seen after adjusting for potential confounders. Our findings support the theory that multiple distinct pathways of tumorigenesis exist in the vicinity of the esophagogastric junction, including one in which tumors arise from dysplastic intestinal metaplasia (intestinal pathway), and one potentially involving dysplasia of the cardiac-type mucosa (non-intestinal pathway). Additional studies are warranted to further clarify their pathogenesis and the molecular mechanisms involved.

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The dichotomy in carcinogenesis of the distal esophagus and esophagogastric junction: intestinal-type vs cardiac-type mucosa-associated adenocarcinoma

et al. 2011

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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.…”

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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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“…In patients with Barrett' s esophagus, adenocarcinoma develops at a rate of 1 in 524 to 1 in 4415 malignancies per patient years. 5,6 Therefore, the progression from simple Barrett' s esophagus without dysplasia to high-grade dysplasia or adenocarcinoma in 9 months is very rapid. In transplant recipients, accelerated progression of dysplastic lesions to carcinoma has been observed in skin cancer 7 and colon cancer.…”

Section: Discussionmentioning

confidence: 99%

Rapid progression to high-grade dysplasia in barrett's esophagus after liver transplantation

Trotter

Brazer

1999

Liver Transpl

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There is an increased incidence of malignancies in transplant recipients. Accelerated progression from a premalignant lesion to carcinoma has been reported in transplant recipients with skin cancer and colon cancer. Whereas Barrett's esophagus is a common premalignant condition in the normal population, rapid progression to severe dysplasia or carcinoma has not been widely reported in transplant recipients. We report on a liver transplant recipient who developed rapid progression from Barrett's esophagus without dysplasia to high-grade dysplasia within 9 months after transplantation.

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Barrett's Esophagus; Development of Dysplasia and Adenocarcinoma

Cited by 801 publications

References 32 publications

The dichotomy in carcinogenesis of the distal esophagus and esophagogastric junction: intestinal-type vs cardiac-type mucosa-associated adenocarcinoma

The dichotomy in carcinogenesis of the distal esophagus and esophagogastric junction: intestinal-type vs cardiac-type mucosa-associated adenocarcinoma

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

Rapid progression to high-grade dysplasia in barrett's esophagus after liver transplantation

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