Barrett's metaplasia and adenocarcinoma of the esophagus and gastroesophageal junction

Thompson, John; Zinsser, Kendall R.; Enterline, Horatio T.

doi:10.1016/s0046-8177(83)80045-8

Cited by 209 publications

(77 citation statements)

References 43 publications

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“…The mucosa represents a complex mixture of cell types and architectural patterns found in the stomach and small intestine [85]. While the various types of epithelium lining Barrett's oesophagus may not be arranged in definite zonal distribution as thought originally [86], it is nevertheless possible to observe discrete areas of gastric metaplasia and intestinal metaplasia.…”

Section: Barrett's Oesophagusmentioning

confidence: 99%

Altered mucin expression in the gastrointestinal tract: a review

Jass

Walsh

2001

J Cellular Molecular Medi

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Early studies of changes in mucin expression in disorders of the gastrointestinal tract focused on alterations in the carbohydrate chain. This review briefly considers the various mechanisms by which such alterations may come about: (a) normal variation, (b) sialic acid alterations, (c) defective assembly of carbohydrate side-chains, (d) changed expression of core proteins and (e) epithelial metaplasia. The availability of monoclonal antibodies to mucin core proteins adds a new dimension to mucin histochemistry. It is now possible to offer explanations for traditional mucin histochemical findings on the basis of lineage-specific patterns of mucin core protein expression. Changes in core protein expression are described in inflammatory, metaplastic and neoplastic disorders of the gastrointestinal tract. The possibility that mucin change could be important in the aetiology of some diseases such as ulcerative colitis and H. pylori gastritis is considered. It is more probable, however, that changes in mucin expression are secondary to reprogramming of cellular differentiation and altered cell turnover. As such they may serve as markers to explain pathogenesis and provide novel diagnostic and prognostic information.

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Section: Barrett's Oesophagusmentioning

confidence: 99%

Altered mucin expression in the gastrointestinal tract: a review

Jass

Walsh

2001

J Cellular Molecular Medi

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“…Three subtypes of BE have been described, but the specialized intestinal type is the only subtype clearly associated with malignant transformation. 6,7 The risk of esophageal adenocarcinoma in patients with BE appears to be approximately 30-to 125-fold greater than that in the general population, with an estimated incidence of 1 in 180 patient-years. 8 -11 Although high-grade dysplasia of BE is generally considered a precursor to invasive carcinoma, the assessment of novel biomarkers and better understanding of the pathophysiology of Barrett's adenocarcinoma may help to identify patients at increased risk for malignant transformation.…”

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confidence: 99%

Molecular Biology of Barrett’s Adenocarcinoma

Wijnhoven

Tilanus²,

Dinjens³

2001

Annals of Surgery

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ObjectiveTo review the current knowledge on the genetic alterations involved in the development and progression of Barrett's esophagus-associated neoplastic lesions. Summary Background DataBarrett's esophagus (BE) is a premalignant condition in which the normal squamous epithelium of the esophagus is replaced by metaplastic columnar epithelium. BE predisposes patients to the development of esophageal adenocarcinoma. Endoscopic surveillance can detect esophageal adenocarcinomas when they are early and curable, but most of the adenocarcinomas are detected at an advanced stage. Despite advances in multimodal therapy, the prognosis for invasive esophageal adenocarcinoma is poor. A better understanding of the molecular evolution of the Barrett's metaplasia to dysplasia to adenocarcinoma sequence may allow improved diagnosis, therapy, and prognosis. MethodsThe authors reviewed data from the published literature to address what is known about the molecular changes thought to be important in the pathogenesis of BE-associated neoplastic lesions. ResultsThe progression of Barrett's metaplasia to adenocarcinoma is associated with several changes in gene structure, gene expression, and protein structure. Some of the molecular alterations already showed promise as markers for early cancer detection or prognostication. Among these, alterations in the p53 and p16 genes and cell cycle abnormalities or aneuploidy appear to be the most important and well-characterized molecular changes. However, the exact sequence of events is not known, and probably multiple molecular pathways interact and are involved in the progression of BE to adenocarcinoma. ConclusionsFurther research into the molecular biology of BE-associated adenocarcinoma will enhance our understanding of the genetic events critical for the initiation and progression of Barrett's adenocarcinoma, leading to more effective surveillance and treatment.Since 1970, the incidence of adenocarcinomas of the esophagus has increased in many countries at a rate that exceeds that of any other malignancy.

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“…The estimated risk of a patient with Barrett's oesophagus developing adenocarcinoma is 30 to 40 times higher than in the general population (Spechler et al, 1984). Tumour development in these patients is proposed to occur via a series of dysplastic cell changes, recognized histologically as a metaplasia-dysplasia-carcinoma sequence (Thompson et al, 1983).…”

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confidence: 99%

Comparison of p53 and DNA content abnormalities in adenocarcinoma of the oesophagus and gastric cardia

Gleeson

Sloan²,

McManus³

et al. 1998

Br J Cancer

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Summary This study examined the association between 1 7p allelic loss, p53 gene mutation, p53 protein expression and DNA aneuploidy in a series of adenocarcinomas arising in the oesophagus and gastric cardia. 1 7p allelic loss was detected in 79% (15 of 19) of oesophageal and in 83% (29 of 35) of gastric adenocarcinomas. p53 mutations were detected in 70% (14 of 20) and 63% (26 of 41) of oesophageal and of gastric adenocarcinomas respectively. Both tumour types were associated with a predominance of base transitions at CpG dinucleotides. In five cases of oesophageal adenocarcinoma, the same mutation was detected both in tumour and in adjacent dysplastic Barrett's epithelium. Diffuse p53 protein expression was detected in 65% (13 of 20) and 59% (24 of 41) of oesophageal and of gastric tumours, respectively, and was associated with the presence of p53 missense mutation (Chi-squared, P < 0.0001). DNA aneuploidy was detected in 80% (16 of 20) of oesophageal and in 70% (28 of 40) of gastric tumours. No association was found between p53 or DNA content abnormalities and tumour stage or histological subtype. In conclusion, this study detected a similar pattern of p53 alterations in adenocarcinoma of the oesophagus and gastric cardia -molecular data consistent with the observation that these tumours demonstrate similar clinical and epidemiological features.

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Barrett's metaplasia and adenocarcinoma of the esophagus and gastroesophageal junction

Cited by 209 publications

References 43 publications

Altered mucin expression in the gastrointestinal tract: a review

Altered mucin expression in the gastrointestinal tract: a review

Molecular Biology of Barrett’s Adenocarcinoma

Comparison of p53 and DNA content abnormalities in adenocarcinoma of the oesophagus and gastric cardia

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