Helicobacter pylori (HP) is a gram negative microaerobic bacterium that colonizes the gastric mucosa. Survival in adverse conditions of acidic gastric medium is enabled by urease synthesis, which catalyses production of ammonia and carbon dioxide from urea and neutralizes gastric pH. Colonization affects nearly half of the global population, with higher prevalence in developing countries, which is why it is related to socioeconomic status. In most cases colonization leads to asymptomatic infection. Long-term infection by HP may result in the development of chronic gastritis. The chronic atrophic gastritis makes the first step in Correa´s cascade, which represents a gradual progression of gastric mucosal changes that lead to the development of gastric carcinoma. That changes include glandular atrophy, intestinal metaplasia and dysplasia of the epitelium. Besides bacterial virulence factors, host properties and environmental factors play an important role in the pathogenesis of gastric carcinoma. Gastric carcinoma is the fifth most common cancer worldwide. Because of clinical symptom absence, and consequently late diagnosis, gastric carcinoma is characterized by high mortality rate. The digestive system is the most common primary site of extranodal non-Hodgkin lymphomas. The stomach makes approximately two-thirds of cases. HP infection represents one of the main risk factors for primary gastric lymphoma (PGL) development. Inflammatory reaction mediated by HP induces B-cell proliferation and lymphoid follicle formation within gastric mucosa. Over time, because of accumulated genetic changes, autonomous growth of B-cell clone occurs and lymphoma develops. In a large number of patients, infection eradication decreases risk for premalignant lesion appearance, and even leads to early stage MALT lymphoma regression. Endoscopy and pathohistological diagnosis present standard procedure in gastric neoplasm finding.