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Foveolar type dysplasia in Barrett esophagus.
Mod Pathol. 2010 Jun; 23(6):834-43.MP

Abstract

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 approximately 27%) dysplasia. Immunohistochemistry confirmed the histological stratification in all cases. Foveolar type dysplasia commonly expressed MUC5AC (P<0.12) but was consistently negative for markers of intestinal differentiation, MUC2, CDX2 and villin (all P<0.01). By contrast, adenomatous type dysplasia frequently displayed intestinal differentiation markers (all P<0.0001) Hybrid-type dysplasia was similar to adenomatous type dysplasia in showing expression of intestinal differentiation markers (P<0.01) 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.

Authors+Show Affiliations

Department of Histopathology, Sullivan Nicolaides Pathology and Royal Brisbane and Women's Hospital Brisbane, Brisbane, Australia. ian_brown@snp.com.auNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20228780

Citation

Brown, Ian S., et al. "Foveolar Type Dysplasia in Barrett Esophagus." Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, vol. 23, no. 6, 2010, pp. 834-43.
Brown IS, Whiteman DC, Lauwers GY. Foveolar type dysplasia in Barrett esophagus. Mod Pathol. 2010;23(6):834-43.
Brown, I. S., Whiteman, D. C., & Lauwers, G. Y. (2010). Foveolar type dysplasia in Barrett esophagus. Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, 23(6), 834-43. https://doi.org/10.1038/modpathol.2010.59
Brown IS, Whiteman DC, Lauwers GY. Foveolar Type Dysplasia in Barrett Esophagus. Mod Pathol. 2010;23(6):834-43. PubMed PMID: 20228780.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Foveolar type dysplasia in Barrett esophagus. AU - Brown,Ian S, AU - Whiteman,David C, AU - Lauwers,Gregory Y, Y1 - 2010/03/12/ PY - 2010/3/16/entrez PY - 2010/3/17/pubmed PY - 2010/9/4/medline SP - 834 EP - 43 JF - Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc JO - Mod. Pathol. VL - 23 IS - 6 N2 - 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 approximately 27%) dysplasia. Immunohistochemistry confirmed the histological stratification in all cases. Foveolar type dysplasia commonly expressed MUC5AC (P<0.12) but was consistently negative for markers of intestinal differentiation, MUC2, CDX2 and villin (all P<0.01). By contrast, adenomatous type dysplasia frequently displayed intestinal differentiation markers (all P<0.0001) Hybrid-type dysplasia was similar to adenomatous type dysplasia in showing expression of intestinal differentiation markers (P<0.01) 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. SN - 1530-0285 UR - https://www.unboundmedicine.com/medline/citation/20228780/Foveolar_type_dysplasia_in_Barrett_esophagus_ L2 - http://dx.doi.org/10.1038/modpathol.2010.59 DB - PRIME DP - Unbound Medicine ER -