Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma

Takubo, Kaiyo; Aida, Junko; Naomoto, Yoshio; Sawabe, Motoji; Arai, Tomio; Shiraishi, Hiroaki; Matsuura, M.; Ell, Christian; May, Andrea; Pech, Oliver; Stolte, Manfred; Vieth, Michael

doi:10.1016/j.humpath.2008.06.008

Cited by 213 publications

(138 citation statements)

References 37 publications

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“…These findings support the notion that two different pathways lead to adenocarcinomas of the distal esophagus and esophagogastric junction: one in which intestinal-type epithelium with goblet cells becomes dysplastic (intestinal pathway) and another in which dysplasia arises in cardiac-type glandular mucosa (non-intestinal pathway). [39][40][41] In contrast, an alternative explanation for the lack of intestinal metaplasia in some adenocarcinomas, 39 overgrowth of short segment intestinal metaplasia by large tumors, 17,42 explains neither the absence of intestinal-type mucosa in certain small esophageal adenocarcinomas 43 nor our observation of phenotypic and molecular differences. Thus, adenocarcinomas of the distal esophagus and esophagogastric junction may be stratified based on the presence or absence of background Barrett mucosa, with unique clinicopathological characteristics in either group, but without significant survival differences.…”

Section: Discussionmentioning

confidence: 58%

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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Section: Discussionmentioning

confidence: 58%

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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“…Two recent studies have suggested the same possibility. 10,46 In a cohort of 712 British patients with endoscopic evidence Barrett esophagus, 44.9% (n ¼ 309) had no microscopic evidence of intestinal metaplasia. Furthermore, 11 patients (3.6%) developed adenocarcinoma, a number not significantly different from the 28 out of 379 patients with intestinal metaplasia.…”

Section: Discussionmentioning

confidence: 99%

“…[7][8][9] However, it is recognized that intestinal metaplasia is not always identified adjacent to invasive adenocarcinoma of the lower esophagus or gastroesophageal junction region. [10][11][12][13][14][15][16][17] Nevertheless, it has been reported that the Barrett esophagus columnar mucosa is 'intestinalized' when examined by immunohistochemical markers of intestinal differentiation, even in the absence of histological evidence of intestinal metaplasia, that is, goblet cells. [18][19][20][21][22][23] Thus supporting the current American College of Gastroenterology guidelines, which require the presence of intestinal metaplasia for the diagnosis of Barrett esophagus.…”

mentioning

confidence: 99%

Foveolar type dysplasia in Barrett esophagus

2010

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Adenocarcinoma of the lower esophagus and esophagogastric junction is increasing in incidence in Western countries. A metaplasia (Barrett esophagus)-dysplasia-carcinoma sequence induced by gastroesophageal reflux disease is established. Two patterns of Barrett dysplasias have been described-adenomatous (type 1) and non-adenomatous (type 2 or foveolar/hyperplastic type). Interestingly, little is known about non-adenomatous dysplasia. Esophagogastrectomy cases from 41 patients with glandular dysplasia with and without associated invasive adenocarcinoma of the lower esophagus were evaluated for expression of MUC2, MUC5AC, CDX2, villin, Ki67 and p53. Results were correlated with sub-classification of the dysplasia into morphologic patterns of adenomatous vs foveolar vs hybrid type. In addition, clinicopathological parameters including the presence and extent of background intestinal metaplasia were also evaluated. Foveolar type dysplasia was present in 46% of the cases and thus, was more common than adenomatous type or hybrid type (both B27%) dysplasia. Immunohistochemistry confirmed the histological stratification in all cases. Foveolar type dysplasia commonly expressed MUC5AC (Po0.12) but was consistently negative for markers of intestinal differentiation, MUC2, CDX2 and villin (all Po0.01). By contrast, adenomatous type dysplasia frequently displayed intestinal differentiation markers (all Po0.0001) Hybrid-type dysplasia was similar to adenomatous type dysplasia in showing expression of intestinal differentiation markers (Po0.01) and therefore could not be sustained as a separate category. In conclusion, our study provides evidence for a non intestinal pathway to neoplastic development in Barrett esophagus, that is, gastric metaplasia-foveolar dysplasia-adenocarcinoma.

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“…Liu et al [36] reported that patients with esophageal columnar metaplasia, but without SIM (goblet cells), showed DNA content abnormalities statistically similar to metaplastic columnar epithelium with SIM. 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 Carcinogenesismentioning

confidence: 97%

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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Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma

Cited by 213 publications

References 37 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

Foveolar type dysplasia in Barrett esophagus

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

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