Absence of either gastric or intestinal phenotype in microscopic differentiated gastric carcinomas

• Published in: The Journal of pathology 2003-04, Vol.199 (4), p.436-446
• Main Authors: Kawachi, Hiroshi, Takizawa, Touichiro, Eishi, Yoshinobu, Shimizu, Shinichiro, Kumagai, Jiro, Funata, Nobuaki, Koike, Morio
• Format: Article
• Language: English
• Subjects: Aged; Biological and medical sciences; CD10; Cell Differentiation; Female; Gastric Mucins - metabolism; Gastric Mucosa - metabolism; Gastric Mucosa - pathology; Gastroenterology. Liver. Pancreas. Abdomen; human gastric mucin; Humans; immunohistochemistry; intestinal metaplasia; Male; Medical sciences; Metaplasia; microscopic gastric carcinoma; Microvilli - metabolism; Microvilli - pathology; Middle Aged; Muc-2; mucin phenotype; Neoplasm Proteins - metabolism; p53 overexpression; Phenotype; Stomach Neoplasms - metabolism; Stomach Neoplasms - pathology; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Tumor Suppressor Protein p53 - metabolism; Tumors
• ISSN: 0022-3417; 1096-9896
• DOI: 10.1002/path.1323

Differentiated gastric carcinoma (DGC) corresponds roughly to the intestinal type of gastric carcinoma described by Laurén. It has been suggested that DGCs arise from intestinalized gastric mucosa, but recent findings regarding their mucin expression do not support this hypothesis. To evaluate the histogenetic relationship between DGCs and intestinal metaplasia, lesions that are as small as possible should be examined. Twenty‐five DGCs, ranging in their greatest dimension from 0.4 to 2.7 mm, were collected and divided into two groups by size. Group A consisted of 13 lesions less than 1.4 mm across, and group B of 12 lesions 1.4 mm or more. The presence of mucin and a brush border was assessed by immunostaining with antibodies against human gastric mucin, pyloric‐gland‐type mucin, Muc‐2 glycoprotein, and CD10 antigen, and the lesions were classified as having the gastric phenotype (G‐type), intestinal phenotype (I‐type), mixed gastric and intestinal phenotype (M‐type), or null phenotype (N‐type). Thirteen (52%) of the 25 lesions were N‐type, 5 (20%) lesions were G‐type, 5 (20%) were I‐type, and 2 (8%) were M‐type. Group A had a larger proportion of N‐type lesions than B (10/13, or 77%, vs. 3/12, or 25%; p = 0.027, chi‐square test for proportions). Group B had a larger proportion of G‐type lesions than A (5/12, or 42%, vs. 0/13, or 0%; p = 0.033). The phenotypes of the carcinomas and their surrounding mucosa were unrelated. Therefore, DGCs may arise from gastric mucosa affected by intestinal metaplasia or not, without having either the gastric or intestinal phenotype. Copyright © 2003 John Wiley & Sons, Ltd.