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.

Residual Embryonic Cells as Precursors of a Barrett's-like Metaplasia

“…Most cases of gastric adenocarcinoma are thought to develop from an “intestine-like” metaplasia very similar to Barrett's that develops from multiple sites in the gastric epithelium secondary to H. pylori infection (Piazuelo et al 2004; Correa and Chen, 1994; Goldenring et al, 2010), though it still remains to be examined whether they too are derived from residual embryonic cells. It is also becoming apparent that pancreatic intraepithelial neoplasia, an intestine-like metaplastic precursor of pancreatic adenocarcinoma, arises from a set of ductal glands expressing embryonic features (Strobel et al, 2010).…”

Helicobacter pyloritargets cancer-associated apical-junctional constituents in gastroids and gastric epithelial cells

“…2425 Gastric biopsies were obtained from H. pylori -infected or uninfected patients residing in Colombia, 26 which was approved by the ethics committees of the participating hospital and the Universidad del Valle in Cali, Colombia, and the institutional review board of Vanderbilt University. Gastric tissue was treated with 10 µM dithiothreitol at room temperature for 30 min and 1.0 mM EDTA for 30 min at 4°C.…”

El fenotipo de las mucinas en el esófago de Barrett

“…Observaciones anteriores en metaplasia intestinal gástrica indican que la metaplasia completa expresa mucinas intestinales, positivas en la tinción de azul Alcian a pH 2,5 y a los anticuerpos contra MUC2, pero no con anticuerpos contra las mucinas gástricas MUC5AC y MUC6 25 . La presencia de islotes de metaplasia completa en nuestros casos de EB podría interpretarse como indicativo de la transformación gradual de metaplasia completa en metaplasia incompleta, tal como se ha descrito en la mucosa gástrica 26 .…”

“…La presencia de islotes de metaplasia completa en nuestros casos de EB podría interpretarse como indicativo de la transformación gradual de metaplasia completa en metaplasia incompleta, tal como se ha descrito en la mucosa gástrica 26 . La presencia de células positivas para anticuerpos contra MUC2 y MUC5AC, en la presente serie, confirma observaciones anteriores que los consideran indicadores de metaplasia intestinal incompleta 25 .…”