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Development of adenocarcinomas in the stomach
Author(s) -
Hattori Takanori
Publication year - 1986
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19860415)57:8<1528::aid-cncr2820570815>3.0.co;2-3
Subject(s) - dysplasia , intestinal metaplasia , histogenesis , adenocarcinoma , pathology , metaplasia , medicine , cancer , stomach , esophagus , carcinoma , gastric mucosa , anatomy , gastroenterology , immunohistochemistry
To elucidate the histogenesis of gastric adenocarcinomas, the author looked for smaller carcinomas, and studied their histologic features and the histologic characteristics of the neighboring gastric mucosa. In 325 resected stomachs, 27 microcarcinomas, including initial lesions, were detected. Most of them were typical adenocarcinomas, whose histologic features were different from those of dysplasias. The gastric mucosa around the microcarcinomas was mostly intestinalized. However, the smaller the carcinomas, the less complete was the form of intestinal metaplasia, and the metaplasia was under progression in many gastric tubules. The smallest carcinomas consisted of a few, newly formed glandular complexes, confined to the neck region of the tubules, whereas the upper and the lower part of the tubules were still lined by normal gastric cells. The smallest dysplasia was an in situ lesion, also confined to the neck region of the tubules. These findings indicate that a starting point of adenocarcinomas and dysplasias is in the proliferative cell zone at the neck region. Intestinal metaplasia, dysplasia, and adenocarcinoma arise coincidentally. This implies that no precursor is present for each of them. It appears that most adenocarcinomas arise in gastric tubules when an abnormal differentiation is induced in stem cells after intestinal metaplasia. They are not a consequence of dysplasia, but share a common origin with it. Cancer 57:1528–1534, 1986.