WORLD JOURNAL OF ADVANCE
HEALTHCARE RESEARCH

Adriana Botezatu* and Nicolae Bodrug

ABSTRACT

The etiology of gastric cancer is complex and multifactorial, involving environmental and host-related factors, as well as genetic and epigenetic changes. Helicobacter pylori infection is necessary but not sufficient for the development of gastric cancer. The annual incidence of gastric cancer is 0.1% in patients with chronic atrophic gastritis, 0.25% in those with gastric intestinal metaplasia, 0.6% in those with mild to moderate gastric epithelial dysplasia, and 6.0% in those with severe gastric epithelial dysplasia within 5 years of diagnosis. The most widely used histological classification of gastric cancer is the Lauren classification, which identifies three subtypes: diffuse (33%, arising from normal gastric mucosa), intestinal (53%, glandular origin and associated with chronic atrophic gastritis and intestinal metaplasia), and mixed (14%). Eradicating H. pylori infection and early detection of precancerous gastric lesions in the general population, along with appropriate treatment and monitoring, are key strategies for prevention, early diagnosis, reduced mortality, improved survival, and enhanced quality of life. Nevertheless, precancerous gastric lesions are frequently overlooked in clinical practice, resulting in variable surveillance and treatment practices and suboptimal risk stratification.