
Expression of MUC2 gene in gastric regenerative, metaplastic, and neoplastic epithelia
Author(s) -
Mitsuuchi Masaki,
Hinoda Yuji,
Itoh Fumio,
Endo Takao,
Satoh Masaaki,
Xing PeiXiang,
Imai Kohzoh
Publication year - 1999
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/(sici)1098-2825(1999)13:6<259::aid-jcla2>3.0.co;2-2
Subject(s) - mucin 2 , intestinal metaplasia , mucin , immunohistochemistry , pathology , epithelium , metaplasia , adenocarcinoma , biology , foveolar cell , paneth cell , cdx2 , stomach , gastric mucosa , gene expression , medicine , cancer , small intestine , dysplasia , gene , biochemistry , genetics , homeobox
It has been reported that MUC2 mucin is expressed in goblet cells of gastric intestinal metaplasia, but not in its normal epithelium. To confirm this finding, we have examined the expression of the MUC2 gene by reverse transcriptase‐polymerase chain reaction and immunohistochemical methods in gastric tissues obtained by routine upper gastrointestinal tract endoscopy and compared the results with pathological findings based on hematoxylin and eosin (H&E) staining. In 16.7% of the tissue specimens tested, MUC2 mRNA was detected in spite of the absence of intestinal metaplasia in HE specimens. A possible explanation for this was the identification by immunohistochemistry of MUC2 protein in regenerative gastric mucosal cells in biopsies that did not contain intestinal metaplasia. Sialyl‐Le x epitope, which is suggested to be located on MUC2 mucin core protein (MUC2 protein), was also immunohistochemically detected in both goblet cells of intestinal metaplasia and regenerative epithelium. With regard to carcinoma, MUC2 protein was predominantly expressed in intestinal‐type adenocarcinoma. These data indicate that MUC2 mucin is expressed in gastric regenerative epithelium in addition to intestinal metaplasia and intestinal type adenocarcinoma. J. Clin. Lab. Anal. 13:259–265, 1999. © 1999 Wiley‐Liss, Inc.