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MUC gene expression and histogenesis of adenocarcinoma of the stomach
Author(s) -
Tsukashita Shizuki,
Kushima Ryoji,
Bamba Masamichi,
Sugihara Hiroyuki,
Hattori Takanori
Publication year - 2001
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.1460
Subject(s) - histogenesis , mucin , pathology , dysplasia , foveolar cell , biology , stomach , adenocarcinoma , adenoma , intestinal metaplasia , goblet cell , immunohistochemistry , carcinoma , mucin 2 , gastric mucosa , cancer , gene expression , medicine , gene , epithelium , genetics , biochemistry
To elucidate the histogenesis of adenocarcinomas of the stomach, we examined MUC gene expression in gland‐forming intramucosal neoplastic lesions. Eighty tumors were histopathologically assigned to 1 of the following 3 groups based upon the Vienna classification: group A (low‐grade adenoma/dysplasia), group B (high‐grade adenoma/dysplasia) and group C (intramucosal carcinoma). Immunohistochemic staining was performed with monoclonal antibodies against MUC2 (goblet cell mucin), MUC5AC (gastric‐foveolar mucin), MUC6 (pyloric‐gland mucin) and CD10 (brush border). Ki‐67 staining was also carried out. An obvious difference existed in MUC gene expression between lesions in group A and those in groups B and C. The majority of group A lesions strongly expressed intestinal markers in which proliferating cell zones were formed but generally expressed no gastric markers, whereas more than 50% of groups B and C tumors expressed gastric markers. These findings suggest that group A lesions are of a stable intestinal phenotype, whereas those in groups B and C are phenotypically and genotypically unstable, indicating that the adenoma‐carcinoma sequence is not a major pathway, but instead that adenocarcinomas arise de novo . © 2001 Wiley‐Liss, Inc.