Gastric carcinogenesis

In most patients, gastric cancer is diagnosed in advanced stage. Curative treatment options are limited and the mortality is high. The process of gastric carcinogenesis is triggered by Helicobacter pylori-driven gastritis and is further characterized by its complexity of interaction with other risk factors. Health care systems are challenged for the improvement of prevention, early diagnosis, and effective treatments.

An extensive literature research has been performed to elucidate the interplay between etiological factors involved in gastric carcinogenesis.

H. pylori is the most important carcinogen for gastric adenocarcinoma. Evidence is provided by experiments including animal studies as well as clinical observational and interventional studies in humans. Eradication has the potential to prevent gastric cancer and offers the greatest benefit if performed before premalignant changes of the gastric mucosa have occurred. Bacterial virulence factors are essential players in modulating the immune response involved in the initiation of the carcinogenesis in the stomach. Host genetic factors contribute to the regulation of the inflammatory response and in the aggravation of mucosal damage. The harmful role of environmental factors is restricted to salt intake and smoking of tobacco. The ingestion of fruit and vegetables has some protective effect.

Infection with H. pylori is the major risk factor for gastric cancer development, and thus, eradication of the Helicobacter offers a promising best option for prevention of the disease. Bacterial virulence, host genetic factors, and environmental influences are interacting in the multifactorial process of gastric carcinogenesis.