Abstract
<jats:p>Helicobacter pylori (H. pylori) is a spiral-shaped, Gram-negative bacterium capable of colonizing the gastric mucosa. Since its discovery in 1982 by Australian scientists Barry Marshall and Robin Warren, it has been recognized as one of the most important factors involved in the development of chronic gastritis, peptic ulcer disease, and, since 1994, gastric cancer. Gastric carcinogenesis involving H. pylori occurs through a multi-step cascade known as the Correa cascade. It includes the transition from chronic non-atrophic gastritis to atrophic gastritis, intestinal metaplasia, dysplasia, and, ultimately, gastric adenocarcinoma. This pathway is characterized by progressive morphological and molecular changes in the gastric mucosa, largely mediated by persistent inflammation and impaired regenerative processes. The main mechanisms of the carcinogenic action of H. pylori include the production of virulence factors (e.g., CagA, VacA), chronic activation of the immune response and oxidative stress, disruption of apoptosis and cell proliferation, epigenetic changes, and DNA damage. As already noted, the presence of H. pylori is recognized as a Class I carcinogen according to the WHO classification, and its eradication is one of the most effective methods of primary prevention of gastric cancer. However, the effectiveness of such prevention depends on many factors, such as the stage of the disease, the timeliness of intervention, adequate therapy, and the presence of concomitant factors, including genetic predisposition and diet.</jats:p>