title: Phenotypic differences between esophageal and gastric intestinal metaplasia.
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: Department of Pathology, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
authors: M Blanca
authors: MB
authors: Piazuelo
authors: Salima
authors: S
authors: Haque
authors: Alberto
authors: A
authors: Delgado
authors: Joanna X
authors: JX
authors: Du
authors: Fred
authors: F
authors: Rodriguez
authors: Pelayo
authors: P
authors: Correa
mesh_terms: D000368:Aged; D000906:Antibodies / Q000032:analysis; D001471:Barrett Esophagus / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D002454:Cell Differentiation; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000473:pathology; D051546:Cyclooxygenase 2 / Q000032:analysis; D004938:Esophageal Neoplasms / Q000737:chemistry / Q000382:microbiology / Q000473:pathology*; D004947:Esophagus / Q000737:chemistry / Q000382:microbiology / Q000473:pathology*; D005260:Female; D016480:Helicobacter pylori / Q000302:isolation & purification; D006801:Humans; D007150:Immunohistochemistry; D018836:Inflammation Mediators / Q000032:analysis; D053554:Keratin-20 / Q000032:analysis; D053552:Keratin-7 / Q000032:analysis; D008145:Louisiana; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D055271:Mucin 5AC; D018396:Mucin-1 / Q000032:analysis; D055262:Mucin-2; D009077:Mucins / Q000032:analysis; D052247:Nitric Oxide Synthase Type II / Q000032:analysis; D010641:Phenotype; D011230:Precancerous Conditions / Q000737:chemistry / Q000382:microbiology / Q000473:pathology*; D013194:Staining and Labeling; D013270:Stomach / Q000737:chemistry / Q000382:microbiology / Q000473:pathology*; D013274:Stomach Neoplasms / Q000737:chemistry / Q000473:pathology*
chemical_list: D000906:Antibodies; C467479:DAS-1 protein, human; D018836:Inflammation Mediators; C507499:KRT20 protein, human; C507497:KRT7 protein, human; D053554:Keratin-20; D053552:Keratin-7; C060192:MUC1 protein, human; C524625:MUC2 protein, human; C524678:MUC5AC protein, human; D055271:Mucin 5AC; D018396:Mucin-1; D055262:Mucin-2; D009077:Mucins; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human