Helicobacter pylori infection is recognized as a major risk factor for the development of gastric cancer, particularly in individuals with long-term and persistent infections. The mechanisms by which H. pylori contributes to gastric carcinogenesis involve chronic inflammation, genetic susceptibility, and bacterial virulence factors. Chronic inflammation induced by H. pylori infection can lead to the gradual transformation of healthy gastric tissue into precancerous lesions and eventually gastric cancer. The bacterium's ability to persistently colonize the stomach and evade the host immune response contributes to the prolonged inflammatory state. Host and bacterial factors play a role in determining the individual's susceptibility to developing gastric cancer following H. pylori infection. Certain strains of H. pylori possess virulence factors, such as the cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA), which are associated with an increased risk of carcinogenesis. Preventing gastric cancer associated with H. pylori infection involves strategies such as early detection and eradication of the bacterium, particularly in high-risk populations. Regular screening and surveillance endoscopy in individuals with persistent H. pylori infection or a family history of gastric cancer can aid in the early identification of precancerous lesions. Efforts to develop an H. pylori vaccine are underway, aiming to reduce the incidence of infection and its associated complications, including gastric cancer. The integration of H. pylori eradication programs, risk stratification, and vaccination strategies holds promise in mitigating the global burden of gastric cancer linked to H. pylori infections.