Gastric cancer remains a major global health problem, with high incidence in East Asia, Eastern Europe and parts of South America. Its development is typically a multistep process that progresses from chronic gastritis to atrophic gastritis, intestinal metaplasia, dysplasia and finally carcinoma. A central cause is infection with Helicobacter pylori, which induces chronic inflammation, genetic damage and alterations in gastric acid secretion. Environmental and lifestyle factors such as high salt intake, smoked and preserved foods, low fruit and vegetable consumption, tobacco use and heavy alcohol intake further increase risk. Genetic predisposition also contributes, including inherited mutations in genes like CDH1, and common variants that subtly alter susceptibility.

Molecular studies reveal that gastric cancer is heterogeneous, comprising distinct subtypes defined by patterns of gene expression, chromosomal instability, microsatellite instability and epigenetic changes. Alterations frequently affect pathways that regulate cell adhesion, growth signaling, DNA repair and immune evasion. These insights have led to the development of targeted therapies, such as drugs inhibiting HER2 or VEGF, and immunotherapies that block immune checkpoints in selected patients. However, the benefits are still limited to subsets of tumors with specific molecular features.

Early detection is critical because prognosis drops sharply once the disease becomes advanced or metastatic. Endoscopic screening programs in high incidence countries have improved survival by identifying early stage lesions. Current research focuses on noninvasive biomarkers from blood, stool or gastric juice, improved imaging techniques, and refined risk stratification models that integrate genetic, microbial and environmental data. Prevention strategies include H. pylori eradication, dietary modifications and tailored surveillance of high risk individuals.