Adenocarcinoma in Barrett's oesophagus: an overrated risk.

Veen, A.H. van der; Dees, Jan; Blankensteijn, Jan D.; Blankenstein, M. van

doi:10.1136/gut.30.1.14

Cited by 203 publications

(77 citation statements)

References 19 publications

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“…Thus, Hsp27 expression in normal oesophagus is unique relative to other heat-shock proteins. BarrettÕs metaplasia is a premalignant lesion associated with an increased risk of adenocarcinoma (Spechler et al, 1984;Van Der Veen et al, 1989). It arises in the setting of long-standing chronic gastro-oesophageal reflux and its attendant oesophagitis and mucosal injury.…”

Section: Discussionmentioning

confidence: 99%

“…BarrettÕs oesophageal metaplasia is a premalignant lesion in which the normal squamous mucosa of the distal oesophagus is replaced by columnar epithelium (Barrett, 1950;Barrett, 1957). It is associated with a 30-to 40-fold increase in the risk of oesophageal adenocarcinoma (Spechler et al, 1984;Van Der Veen et al, 1989), which develops in approximately 10% of patients with BarrettÕs metaplasia (Naef et al, 1975). BarrettÕs metaplasia is commonly thought to arise as a consequence of chronic gastro-oesophageal reflux-induced injury (Goldman and Beckman, 1960;Bremner et al, 1970).…”

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confidence: 99%

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Differential expression of Hsp27 in normal oesophagus, Barrett’s metaplasia and oesophageal adenocarcinomas

et al. 1999

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SummaryThe protein expression patterns of normal, metaplastic and malignant oesophageal tissues were analysed by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) to identify changes associated with Barrett's metaplasia and transformation to oesophageal adenocarcinoma. Heat-shock protein 27 (Hsp27), a small heat-shock protein which is protective against cytotoxic stresses, was abundant in normal oesophagus. However, Hsp27 expression was markedly lower in Barrett's metaplasia and oesophageal adenocarcinomas. This was confirmed by immunohistochemical analysis. Hsp27 protein was most highly expressed in the upper layers of squamous epithelium and exhibited a pattern of expression that corresponded with the degree of squamous maturation. Northern and Southern analysis demonstrated Hsp27 to be regulated at the level of mRNA transcription or abundance. Normal oesophageal tissues were examined for gender differences in Hsp27 expression. Women expressed fourfold higher levels of Hsp27 mRNA, however, this difference was not appreciable in protein expression. Hsp27 protein was inducible by heat shock in Barrett's adenocarcinoma cell lines and an immortalized oesophageal epithelial cell line (HET-1A), but not by oestradiol. These results demonstrate abundant constitutive expression of the stress-response protein Hsp27 in the normal oesophagus, and suggest that low-level expression in Barrett's metaplasia may be one factor which may influence susceptibility to oesophageal adenocarcinoma development.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Differential expression of Hsp27 in normal oesophagus, Barrett’s metaplasia and oesophageal adenocarcinomas

et al. 1999

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“…B arrett's oesophagus is recognised as a premalignant condition, with the incidence of adenocarcinoma in those with Barrett's being much higher than in the general population. There have been at least 27 cohort studies with relative risk estimates varying from as low as 30-fold 27 to more than 500-fold. 18 Most have been based on relatively small numbers of cancers developing (maximum eight cancers) and of years of follow up.…”

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confidence: 99%

Risk of oesophageal cancer in Barrett's oesophagus and in gastro-oesophageal reflux

Solaymani‐Dodaran¹,

Coupland²,

Logan³

2003

Gastroenterology

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Background and aims: While patients with Barrett's oesophagus develop oesophageal adenocarcinoma more frequently than the general population, it has controversially been suggested that gastrooesophageal reflux (GORD) itself is a more important determinant of risk. In order to assess the validity of this suggestion, we examined the risk of oesophageal cancer in patients with Barrett's and with GORD compared with the general population in a community based cohort study. Methods: Cohorts of patients with Barrett's (n = 1677), oesophagitis (n = 6392), and simple reflux (n = 6328), and a reference cohort (n = 13416) were selected from the General Practice Research Database. The last three cohorts were matched to the Barrett's cohort by general practitioner practice, age, and sex. Cox's regression analysis was used to calculate relative risks for oesophageal cancer. Standardised incidence ratio methodology was used to estimate the relative risks for oesophageal adenocarcinoma. Results: A total of 137 oesophageal cancers were identified, of which 94 prevalent cases were excluded. The hazard ratios for oesophageal cancer were 10.6 (5.1-22.0), 2.2 (0.9-5.2), and 1.7 (0.7-4.5) in the Barrett's, oesophagitis, and reflux cohorts compared with the reference cohort, respectively. The corresponding relative risks for oesophageal adenocarcinoma were 29.8 (9.6-106), 4.5 (1.04-19.6), and 3.1 (0.6-14.2). Conclusion: Barrett's oesophagus increases the risk of oesophageal cancer approximately 10 times and oesophageal adenocarcinoma approximately 30 times compared with the general population. There is only a modestly increased risk of oesophageal cancer in patients with reflux who have no record of Barrett's oesophagus. Our findings therefore do not support the suggestion that gastro-oesophageal reflux disease itself predisposes to cancer.

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“…This condition is associated with a 30-40 times increased risk of developing esophageal adenocarcinoma (32,37). Even after surgical resection and/or radiotherapy and chemotherapy, Barrett's adenocarcinoma has a poor prognosis (15).…”

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Detection of genetic changes in Barrett's adenocarcirioma and Barrett's esophagus by DNA in situ hybridization and immunohistochemistry

Krishnadath

Tilanus

Alers³

et al. 1994

Cytometry

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We have investigated the occurrence of chromosomal DNA and cell cycle‐related protein changes in Barrett's epithelium and adenocarcinoma. The presence of numerical chromosomal aberrations was studied by applying nonisotopic in situ hybridization (ISH) with (peri‐)centromeric DNA probes, specific for chromosomes 7, 8, 17, and Y, to routinely processed tissue sections of five cases (4 male, 1 female) of Barrett's adenocarcinoma and adjacent Barrett's epithelium. Cell cycle‐related protein expression was studied by immunohistochemistry (IHC) for p53 protein and the Ki‐67 antigen (Mib‐1) in subsequent sections. P53 protein overexpression was found in 3 of the 5 tumors. Overrepresentation of chromosome 8 and loss of chromosome 17 were found in 2 adenocarcinomas, both also negative for p53 protein overexpression. Y‐loss, mostly clonal, was detected in 3 of the 4 male adenocarcinomas and 2 cases of adjacent Barrett's epithelium. One tumor had both areas of overrepresentation and loss of the Y chromosome. All Barrett's adenocarcinomas appeared to contain aneuploid cell populations. No relation was found between cell proliferation characteristics and chromosomal aberrations. We conclude that ISH with chromosome specific DNA probes can be applied for the assessment of potentially important numerical chromosome changes in Barrett's esophagus. Further, the combination of IHC and ISH is useful for evaluation of specific genetic events. © 1994 Wiley‐Liss, Inc.

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Adenocarcinoma in Barrett's oesophagus: an overrated risk.

Cited by 203 publications

References 19 publications

Differential expression of Hsp27 in normal oesophagus, Barrett’s metaplasia and oesophageal adenocarcinomas

Differential expression of Hsp27 in normal oesophagus, Barrett’s metaplasia and oesophageal adenocarcinomas

Risk of oesophageal cancer in Barrett's oesophagus and in gastro-oesophageal reflux

Detection of genetic changes in Barrett's adenocarcirioma and Barrett's esophagus by DNA in situ hybridization and immunohistochemistry

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