Implication of duodenogastric reflux in the pathogenesis of Barrett's oesophagus

Gillen, P.; Keeling, P. W. N.; Byrne, Patrick J.; Healy, Marie-Louise; O’Moore, R. R.; Hennessy, T. P. J.

doi:10.1002/bjs.1800750612

Cited by 173 publications

(76 citation statements)

References 12 publications

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“…cholic acid or conjugated bile acids (32). The present data therefore suggest a plausible mechanism to explain the promotion of esophageal (42)(43)(44) and colon (24 -27) cancer by bile acids: induction of COX-2.…”

Section: Discussionmentioning

confidence: 55%

Dihydroxy Bile Acids Activate the Transcription of Cyclooxygenase-2

Zhang¹,

Subbaramaiah²,

Altorki³

et al. 1998

Journal of Biological Chemistry

188

125

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Section: Discussionmentioning

confidence: 55%

Dihydroxy Bile Acids Activate the Transcription of Cyclooxygenase-2

Zhang¹,

Subbaramaiah²,

Altorki³

et al. 1998

Journal of Biological Chemistry

188

125

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“…However, the cohlmnar epithelium of Barrett's oesophagus has also been reported to occur after total gastrectomy in which there is no gastnc juice to reflux into the oesophagus (Meyer et al, 1979;Sandvik & Havorsen, 1988). Other recent studies (Gillen et al, 1988;Waring et al, 1990) showed that patients with columnar-lined lower oesophagus epithelial metaplasia have higher bile acid levels in the stomach than do either patients with reflux oesophagitis without columnar-lined epithelium or normal individuals. The development of complications (stricture, ulceration and dysplasia) in Barrett's oesophagus are suggested to be related to aliah gastro-oesophageal reflux (Attwood et al, 1989).…”

Section: Pathologymentioning

confidence: 92%

“…This columnarlined epithelium develops in response to gastro-oesophageal reflux (Mossberg, 1966;Halvorsen & Semp, 1975;Gillen et al, 1988;Seabrook et al, 1992). Thus, the association of adenocarcinoma with gastro-oesophageal reflux is well established.…”

mentioning

confidence: 99%

Induction of oesophageal and forestomach carcinomas in rats by reflux of duodenal contents

Miwa

Segawa²,

Takano³

et al. 1994

Br J Cancer

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S_mmmmary A study was designed to determine whether oesophageal carcinomas can be induced through reflux of duodenal contents. Male Wistar rats weighing 230 -250 g were divided into three groups according to the surgical procedure performed: (1) the duodenal contents were directed into the forestomach through a stoma (duodeno-forestomach reflux); (2) the duodenal contents were regurgitated into the forestomach through the glandular stomach (duodeno-glandular-forestomach reflux); and (3) a sham operation was performed as a control. Animals were fed standard CRF-1 solid food and tap water that was not exposed to carcinogens and were sacrificed 50 weeks post-operatively. While no neoplasia was observed in any of the 32 control rats, 4/11 (36%) with duodeno-forestomach reflu.x and 3/18 (17%) animals with duodeno-glandular-forestomach reflux developed carcinomas in the lower oesophagus and forestomach. The incidence in each group was significantly higher than in the controls (P<0.01 and P<0.05 respectively). Six of the seven lesions consisted of squamous cell carcinomas, and one was a mucinous adenocarcinoma. Oesophageal columnar epithelial metaplasia was observed in two (18%) of the animals with duodeno-forestomach reflux. Carcinomas were always surrounded by chronic inflammatory changes, including regenerative thickening, basal cell hyperplasia and dysplasia. Additional well-differentiated adenocarcinomas were observed in the prepyloric antrum of 6/18 (33%) animals with duodeno-glandular-forestomach reflux. These findings indicate that chronic reflux of duodenal contents may cause oesophageal carcinoma.Oesophageal adenocarcinoma frequently occurs in the lower oesophagus, in the bed of the columnar-lined epithelium (Barrett's oesophagus) (Naef et al., 1975;McDonald et al., 1977; Witt et al., 1983;Miros et al., 1991). This columnarlined epithelium develops in response to gastro-oesophageal reflux (Mossberg, 1966;Halvorsen & Semp, 1975;Gillen et al., 1988; Seabrook et al., 1992). Thus, the association of adenocarcinoma with gastro-oesophageal reflux is well established. However, there are few data indicating whether squamous cell carcinoma, by far the most frequent type of oesophageal carcinoma, may also occur as a result of reflux. Some clinical evidence supports this assumption. Individuals with a history of gastrectomy occasionally develop squamous cell carcinomas in the lower oesophagus, probably as a consequence of post-surgical reflux oesophagitis (Shearman et al., 1970;Rossi et al., 1984;Maeta et al., 1990;Seto et al., 1991). Long-lasting reflux oesophagitis following oesophageal hiatus hernia is known to be closely related to the occurrence of oesophageal cancer (Kuylenstierna & Munck-Wikland, 1985). Epidemiological studies reveal that a form of chronic oesophagitis, which is thought to result from nutritional deficiencies, is the most frequent lesion found in populations at high risk of oesophageal cancer in such areas as Kashmir in India, southern Africa, northern Iran and Linxian and Huixian in China (Cres...

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“…8,9 The origin and pathological progression of BE and the contribution of gastroesophageal reflux in the disease process have been extensively studied in animal models. 1,[10][11][12][13] The metaplastic process of BE appears to be a protective adaptation 14 or a regenerative healing mechanism. 15 It is hypothesized that 'pleuripotent cells' from the native esophageal stratified squamous epithelium or ductal epithelium of the esophageal submucosal glands may give rise to the specialized columnar epithelium.…”

mentioning

confidence: 99%

Repeated exposure to acid and bile selectively induces colonic phenotype expression in a heterogeneous Barrett's epithelial cell line

Bajpai

Liu

Geng

et al. 2008

Laboratory Investigation

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Barrett's epithelium is a precancerous, specialized columnar metaplasia in the distal esophagus. We demonstrate the changes in cellular phenotype in a non-neoplastic Barrett's cell line (BAR-T), following exposure to acid and bile salt, the two important components of gastroesophageal refluxate. Cell phenotypes in BAR-T cell line were quantified by fluorescence-activated cell sorting (FACS) using monoclonal antibodies against markers: cytokeratin 8/18 (CK8/18) for columnar, CK4 for squamous, mAbDas-1 for colonic epithelial cell phenotype and p75NTR for esophageal progenitors. Cells were exposed for 5 min each day to 200 mM glycochenodeoxycholic acid at pH 4, pH 6 and pH 7.4 or only to acid (pH 4) for up to 6 weeks. The BAR-T cell line comprised 35 ± 5.2% CK8/18, 32 ± 3.5% mAbDas-1, 9.5 ± 3% CK4 and 4 ± 2.5% p75NTR-positive cells. Single exposure to acid and or bile did not change cell phenotypes. However, chronic treatment for at least 2 weeks significantly enhanced (Po0.05) the expression of colonic phenotype and CK8/18-positive cells, as evidenced by FACS analysis. Bile salt at pH 4 and bile salt followed by acid (pH 4) in succession were the strongest stimulators (Po0.01) for induction of colonic phenotype cells. Squamous (CK4 þ ) phenotype did not change by the treatments. Cox-2 expression was induced after acute treatment and increased to twofold during chronic treatment, particularly in response to acidic pH. We conclude that BAR-T cells can be utilized as an 'in vitro' model to study the effect of environmental factors and their influence on the cellular phenotype and molecular changes in the pathogenesis of esophageal cancer.

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Implication of duodenogastric reflux in the pathogenesis of Barrett's oesophagus

Cited by 173 publications

References 12 publications

Dihydroxy Bile Acids Activate the Transcription of Cyclooxygenase-2

Dihydroxy Bile Acids Activate the Transcription of Cyclooxygenase-2

Induction of oesophageal and forestomach carcinomas in rats by reflux of duodenal contents

Repeated exposure to acid and bile selectively induces colonic phenotype expression in a heterogeneous Barrett's epithelial cell line

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