Adenocarcinoma developes in the "cirrhotic" not just atrophic gastric mucosa

Helicobacter pylori has been postulated as a group 1 carcinogen, but the mechanism of gastric carcinogenesis remains to be elucidated. It is believed that gastric cancer morphogenesis follows Correa's paradigm of a gastritis-->atrophy-->metaplasia-->dysplasia-->cancer sequence. The aim of the present study was to investigate by histology non-cancerous gastric mucosa in early gastric cancer. Forty cases of early gastric cancer were collected from the files. In all cases of well differentiated adenocarcinoma mucosal atrophy and intestinal metaplasia were present in non-cancerous gastric mucosa. In addition, focal glandular hyperplasia was present in 83.3% of cases and hyperplastic surface epithelium was present in 50% of cases. Mucosal atrophy and intestinal metaplasia were seen in 90.5% of poorly differentiated adenocarcinomas. This was accompanied by surface epithelium hyperplasia in 66.7% and glandular hyperplasia in 47.6% of cases. In a diffuse early gastric cancer atrophy was present in 71.4%, intestinal metaplasia in 57.1%, while hyperplasia (either surface epithelium or glandular) was present in 42.8%. With the introduction of Genta's "strict definition" of gastric mucosal atrophy it became clear that atrophic gastric mucosa is not just a case of simple atrophy but can be in some respect compared to a cirrhotic organ.