Gastric cancer, or stomach cancer, remains a major global cause of cancer death, especially in East Asia, Eastern Europe and parts of South America. Incidence is strongly linked to infection with Helicobacter pylori, dietary patterns, smoking and genetic predisposition.

Research shows that H. pylori is a key driver of chronic inflammation in the gastric mucosa, which can progress through atrophy, intestinal metaplasia and dysplasia to carcinoma. Not everyone with H. pylori develops cancer, so host genetics, bacterial virulence factors and environmental cofactors are important. Eradication of H. pylori with antibiotics can significantly reduce cancer risk, especially when done before precancerous changes become advanced.

Dietary factors play a central role. High intake of salted, smoked and preserved foods, as well as nitrite containing processed meats, increases risk, while fresh fruits and vegetables appear protective through antioxidant and micronutrient effects. High salt also seems to exacerbate H. pylori mediated damage.

Genetic studies have identified polymorphisms in inflammatory pathway genes and in DNA repair and cell cycle regulators that modify individual susceptibility. Hereditary diffuse gastric cancer, often linked to germline CDH1 mutations, exemplifies a high risk inherited form in which prophylactic gastrectomy is sometimes recommended.

Molecular characterization of tumors has revealed distinct subtypes defined by patterns of mutations, chromosomal instability, microsatellite instability and Epstein Barr virus positivity. These subtypes have prognostic and therapeutic implications and are guiding development of targeted and immune based treatments.

Overall, current research emphasizes early detection, H. pylori control, modification of diet and smoking, and precision oncology approaches tailored to tumor biology.