title: Histopathological phenotypes of early gastric cancer and its background mucosa.
abstract: Recent advances in endoscopic submucosal dissection (ESD) techniques contribute to endoscopic treatment of early gastric cancer (EGC). Recognition of chronic atrophic gastritis as the background is important for high-quality detection and diagnosis of EGC. But, relationships between EGC and atrophy of the background gastric mucosa caused by Helicobacter pylori are not well understood. The present study demonstrated histopathological phenotypes of EGC, as well as chronic atrophic gastritis as background mucosa of EGC. We evaluated mucosal heights, number of glands, and degree of intestinal metaplasia (IM) of the background gastric mucosa, using 81 cases of EGC resected by ESD. Gastric phenotype cancer cases showed IM of the background gastric mucosa less frequently, compared with intestinal phenotype cancer cases (score of IM, 1.15 vs. 1.65, P = 0.012). The average mucosal heights around EGC were lower in moderately to poorly differentiated adenocarcinoma cases than well differentiated adenocarcinoma cases (442.6 µm vs. 500.2 µm, P = 0.011). The mucosal atrophy indicated by average heights of background mucosa was low in the gastric phenotype cancer cases, compared with the intestinal phenotype cancercases (452.8 µm vs. 505.6 µm, P = 0.018). In the fundic gland area, the mucosal heights were low in the gastric phenotype cancer cases, compared with the intestinal phenotype cancer cases (413.2 µm vs. 495.5 µm, P = 0.015). Our results using EGC specimens indicated that gastric phenotype cancer and moderately to poorly differentiated adenocarcinoma had atrophic background mucosa with lower mucosal heights and less IM. The atrophic gastric mucosa with less IM is thought to play an important role in gastric carcinogenesis, especially tumoriogenesis of gastricphenotype cancer.
authors.affiliation: Departments of Pathology and Bioscience, Hirosaki University Graduates School of Medicine, Zaifu-cho, Hirosaki, Aomori, Japan.
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Kudo
authors.forename: Satoko
authors.initials: S
authors.lastname: Morohashi
authors.forename: Kaori
authors.initials: K
authors.lastname: Takasugi
authors.forename: Shinji
authors.initials: S
authors.lastname: Tsutsumi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ogasawara
authors.forename: Norihiro
authors.initials: N
authors.lastname: Hanabata
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Yoshimura
authors.forename: Fuyuki
authors.initials: F
authors.lastname: Sato
authors.forename: Shinsaku
authors.initials: S
authors.lastname: Fukuda
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kijima
mesh_terms: D000230:Adenocarcinoma / Q000473:pathology; D000368:Aged; D001284:Atrophy / Q000473:pathology; D002471:Cell Transformation, Neoplastic / Q000473:pathology; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology*; D005757:Gastritis, Atrophic / Q000150:complications / Q000473:pathology*; D016481:Helicobacter Infections / Q000382:microbiology / Q000473:pathology; D016480:Helicobacter pylori / Q000502:physiology; D006801:Humans; D007414:Intestinal Neoplasms / Q000473:pathology*; D007422:Intestines / Q000473:pathology; D007564:Japan; D008297:Male; D008679:Metaplasia / Q000473:pathology; D011230:Precancerous Conditions / Q000473:pathology; D013270:Stomach / Q000473:pathology; D013274:Stomach Neoplasms / Q000473:pathology*