Barrett's oesophagus: Intestinal metaplasia is not essential for cancer risk

Kelty, C; Gough, Martin; Wyk, Quintin Van; Stephenson, T.J.; Ackroyd, Roger

doi:10.1080/00365520701420735

Cited by 200 publications

(116 citation statements)

References 29 publications

(14 reference statements)

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“…In an interesting clinical study by Takubo et al [38], it was revealed that 71 % of BE patients had cardiatype epithelium, not SIM, found adjacent to tiny EAC, and 57 % had no SIM as detected in the specimen by endoscopic resection. Other studies indicated a similar finding, i.e., that non-SIM BE mucosa has the same cancer risk as that of intestinal-type mucosa [39][40][41].…”

Section: Sim (Goblet Cells) and Carcinogenesissupporting

confidence: 61%

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

Watari

Oshima

Fukui

et al. 2013

Clin J Gastroenterol

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Barrett's esophagus (BE) is a premalignant condition of esophageal adenocarcinoma (EAC). Although the incidence of BE has risen rapidly in the West, it is rare in Asia despite a recent increase in the prevalence of gastroesophageal reflux disease. Controversies over the definition of BE are presented because most cases show shortsegment BE, especially ultra-short BE, in Asia. Here we review possible risk factors for the development of EAC, particularly possible roles of ethnicity, specialized intestinal metaplasia (SIM), BE length, and environmental factors, such as Helicobacter pylori infection and obesity. Additionally, we summarize recent studies on the effect of chemoprevention including proton pump inhibitors, nonsteroidal anti-inflammatory drugs or aspirin in order to reduce the risk of neoplastic progression in BE patients. Although substantial knowledge of risk factors of dysplasia/EAC in BE is shown, the risk for neoplastic development may be influenced by geographic variation, study population, the presence or absence of SIM or dysplasia at baseline, and the small number of BE patients investigated. Recently, the efficiency of surveillance for BE patients has been discussed from the standpoint of cost-effectiveness. It may be too difficult to draw conclusions because no randomized clinical trials of BE surveillance have been performed.

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Section: Sim (Goblet Cells) and Carcinogenesissupporting

confidence: 61%

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

Watari

Oshima

Fukui

et al. 2013

Clin J Gastroenterol

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“…Large population-based cohort studies have demonstrated a substantially lower EAC risk in subjects with columnar metaplasia without IM compared with those with IM ( 11 ). However, not all studies have corroborated this fi nding ( 12 ). Although DNA content abnormalities appear to be comparable in both metaplastic epithelium without goblet cells compared with metaplastic epithelium with goblet cells, other studies suggest that cancer most commonly occurs in columnar metaplasia with goblet cells compared with columnar metaplasia without goblet cells ( 11,13,14 ).…”

Section: Summary Of Evidencementioning

confidence: 89%

ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus

Shaheen

Falk

Iyer

et al. 2016

American Journal of Gastroenterology

1,317

1,387

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Recent population studies suggest that gastroesophageal refl ux disease (GERD) is increasing in prevalence, both in the United States and worldwide ( 1,2 ). Th e diagnosis of GERD is associated with a 10-15% risk of Barrett's esophagus (BE), a change of the normal squamous epithelium of the distal esophagus to a columnar-lined intestinal metaplasia (IM). Risk factors associated with the development of BE include long-standing GERD, male gender, central obesity ( 3 ), and age over 50 years ( 4,5 ). Th e goal of a screening and surveillance program for BE is to identify individuals at risk for progression to esophageal adenocarcinoma (EAC), a malignancy that has been increasing in incidence since the 1970s ( 6,7 ).Th e purpose of this guideline is to review the defi nition and epidemiology of BE, available screening modalities for BE detection, rationale and methods for surveillance, and available treatment modalities including medical, endoscopic, and surgical techniques. In order to evaluate the level of evidence and strength of recommendations, we used the GRADE (Grading of Recommendations Assessment, Development and Evaluation) system ( 8 ). Th e level of evidence ranged from "high" (implying that further research was unlikely to change the authors' confi dence in the estimate of the eff ect) to "moderate" (further research would be likely to have an impact on the confi dence in the estimate of eff ect) to "low" (further research would be expected to have an important impact on the confi dence in the estimate of the eff ect and would be likely to change the estimate) or "very low" (any estimate of eff ect is very uncertain). Th e strength of a recommendation was graded as "strong" when the desirable eff ects of an intervention clearly outweighed the undesirable eff ects and as "conditional" when there was uncertainty about the tradeoff s. We used meta-analyses or systematic reviews when available, followed by clinical trials and cohort and case-control studies. In order to determine the level Barrett's esophagus (BE) is among the most common conditions encountered by the gastroenterologist. In this document, the American College of Gastroenterology updates its guidance for the best practices in caring for these patients. These guidelines continue to endorse screening of high-risk patients for BE; however, routine screening is limited to men with refl ux symptoms and multiple other risk factors. Acknowledging recent data on the low risk of malignant progression in patients with nondysplastic BE, endoscopic surveillance intervals are attenuated in this population; patients with nondysplastic BE should undergo endoscopic surveillance no more frequently than every 3-5 years. Neither routine use of biomarker panels nor advanced endoscopic imaging techniques (beyond high-defi nition endoscopy) is recommended at this time. Endoscopic ablative therapy is recommended for patients with BE and high-grade dysplasia, as well as T1a esophageal adenocarcinoma. Based on recent level 1 evidence, endoscopic ablative therapy is ...

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“…This was not statistically different from the 7.4% of patients with Barrett esophagus who developed adenocarcinoma. 59 On the basis of these results, it is reasonable to speculate that metaplastic columnar epithelium without intestinal metaplasia (gastric/cardiac type metaplasia) in the distal esophagus and esophagogastric junction is not uncommon, especially in the older population, and could be a precursor to the non-intestinal-type adenocarcinoma. Therefore, our results, if confirmed, would support the recent recommendation of AGA that defines 'Barrett esophagus' as the condition in which any extent of metaplastic columnar epithelium (irrespective of the presence of goblet cells) that predisposes to cancer development replaces the native squamous epithelium of the distal esophagus, 60 and could be the basis for challenging the current surveillance protocol.…”

Section: Discussionmentioning

confidence: 87%

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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Barrett's oesophagus: Intestinal metaplasia is not essential for cancer risk

Abstract: Patients who have glandular mucosa on biopsy without intestinal metaplasia have a similar cancer risk to those with specialized intestinal metaplasia.

Cited by 200 publications

References 29 publications

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus

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

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