Gastric Cancer
Chronic Helicobacter pylori infection drives atrophic gastritis and intestinal metaplasia, and it is this field of pre-malignant change accumulating over years (not a single event) that eventually gives rise to adenocarcinoma, which is why early disease is silent and presentation is often late.
First principles
Why chronic inflammation, not a single insult, causes gastric cancer
H. pylori colonises the gastric antral mucosa and provokes a chronic active gastritis. Sustained over years, this inflammation progresses through a recognised sequence: chronic gastritis, then atrophic gastritis (loss of normal glandular mucosa), then intestinal metaplasia, then dysplasia, then adenocarcinoma (the Correa cascade). Other risk factors (smoking, a high-salt or nitrate-rich diet, pernicious anaemia, and a family history) act on the same inflammatory pathway rather than through separate mechanisms, which is why gastric cancer is best understood as the end point of a field of chronic mucosal change rather than a single mutation.
Educational content pending clinical review. Not medical advice.