Inflammation, atrophy, and gastric cancer
J. Clin. Invest. James G. Fox, et al. 117:60 doi:10.1172/JCI30111 [Go to this article.]

Figure 2
Proposed Correa pathway of pathological events in gastric adenocarcinoma. In well-differentiated, intestinal-type gastric cancer, histopathological studies indicated that chronic H. pylori infection progresses over decades through stages of chronic gastritis, atrophy, intestinal metaplasia, dysplasia, and cancer (123). The development of cancer has been attributed to alterations in DNA caused by chronic inflammation, recruitment and engraftment of bone marrow–derived cells, an imbalance between epithelial cell proliferation and apoptosis, and, in a milieu of atrophy and achlorhydria, gastric colonization by enteric bacteria with nitrate reductase activity, which facilitates the formation of carcinogenic nitrosamines. Corpus-predominant atrophy, or the loss of specialized glandular cell types such as parietal and chief cells, appears to be the critical initiating step in the progression toward cancer. Adapted with permission from the New England Journal of Medicine (14).