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Phenotypic differences between esophageal and gastric intestinal metaplasia.
Mod Pathol. 2004 Jan; 17(1):62-74.MP

Abstract

Intestinal metaplasia is a cancer precursor in the esophagus and the stomach. Marked differences exist between the carcinogenic processes in the two locations in terms of natural history and clinical significance. We investigated biopsies from 52 patients with Barrett's esophagus and from 50 patients with gastric intestinal metaplasia in an attempt to throw light on their pathogenic processes. Morphologic characteristics, presence of Helicobacter pylori (H. pylori), and markers of differentiation, inflammation, and proliferation were evaluated by histochemical and immunohistochemical techniques. The area covered by incomplete type of intestinal metaplasia and the proportion of sulfomucins were significantly higher in the esophagus than in the stomach. Immunoreactivity with MUC1, MUC2, MUC5AC, Das-1, cytokeratins 7 and 20, inducible nitric oxide synthase and cyclooxygenase-2 antibodies was also significantly greater in Barrett's esophagus than in gastric intestinal metaplasia. In gastric intestinal metaplasia, the presence of MUC1, MUC5AC, Das-1 and cytokeratin 7 was restricted to areas with the incomplete type of metaplasia. Cell proliferation (Ki-67) was significantly higher in Barrett's esophagus than in gastric intestinal metaplasia. H. pylori was absent in all of the patients with Barrett's esophagus, while it was present in 70% of the patients with gastric intestinal metaplasia. Our observations made clear that Barrett's esophagus shares some phenotypic characteristics with gastric intestinal metaplasia, leading us to suggest that both could arise in response to injuries with eventual carcinogenic potential. However, the progression to more advanced lesions could be modulated by the nature of the carcinogenic insult.

Authors+Show Affiliations

Department of Pathology, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

14631367

Citation

Piazuelo, M Blanca, et al. "Phenotypic Differences Between Esophageal and Gastric Intestinal Metaplasia." Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, vol. 17, no. 1, 2004, pp. 62-74.
Piazuelo MB, Haque S, Delgado A, et al. Phenotypic differences between esophageal and gastric intestinal metaplasia. Mod Pathol. 2004;17(1):62-74.
Piazuelo, M. B., Haque, S., Delgado, A., Du, J. X., Rodriguez, F., & Correa, P. (2004). Phenotypic differences between esophageal and gastric intestinal metaplasia. Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, 17(1), 62-74.
Piazuelo MB, et al. Phenotypic Differences Between Esophageal and Gastric Intestinal Metaplasia. Mod Pathol. 2004;17(1):62-74. PubMed PMID: 14631367.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Phenotypic differences between esophageal and gastric intestinal metaplasia. AU - Piazuelo,M Blanca, AU - Haque,Salima, AU - Delgado,Alberto, AU - Du,Joanna X, AU - Rodriguez,Fred, AU - Correa,Pelayo, PY - 2003/11/25/pubmed PY - 2008/5/10/medline PY - 2003/11/25/entrez SP - 62 EP - 74 JF - Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc JO - Mod. Pathol. VL - 17 IS - 1 N2 - Intestinal metaplasia is a cancer precursor in the esophagus and the stomach. Marked differences exist between the carcinogenic processes in the two locations in terms of natural history and clinical significance. We investigated biopsies from 52 patients with Barrett's esophagus and from 50 patients with gastric intestinal metaplasia in an attempt to throw light on their pathogenic processes. Morphologic characteristics, presence of Helicobacter pylori (H. pylori), and markers of differentiation, inflammation, and proliferation were evaluated by histochemical and immunohistochemical techniques. The area covered by incomplete type of intestinal metaplasia and the proportion of sulfomucins were significantly higher in the esophagus than in the stomach. Immunoreactivity with MUC1, MUC2, MUC5AC, Das-1, cytokeratins 7 and 20, inducible nitric oxide synthase and cyclooxygenase-2 antibodies was also significantly greater in Barrett's esophagus than in gastric intestinal metaplasia. In gastric intestinal metaplasia, the presence of MUC1, MUC5AC, Das-1 and cytokeratin 7 was restricted to areas with the incomplete type of metaplasia. Cell proliferation (Ki-67) was significantly higher in Barrett's esophagus than in gastric intestinal metaplasia. H. pylori was absent in all of the patients with Barrett's esophagus, while it was present in 70% of the patients with gastric intestinal metaplasia. Our observations made clear that Barrett's esophagus shares some phenotypic characteristics with gastric intestinal metaplasia, leading us to suggest that both could arise in response to injuries with eventual carcinogenic potential. However, the progression to more advanced lesions could be modulated by the nature of the carcinogenic insult. SN - 0893-3952 UR - https://www.unboundmedicine.com/medline/citation/14631367/Phenotypic_differences_between_esophageal_and_gastric_intestinal_metaplasia_ L2 - http://dx.doi.org/10.1038/sj.modpathol.3800016 DB - PRIME DP - Unbound Medicine ER -