A comprehensive review study on the association between Helicobacter pylori infection and gastric Cancer

Helicobacter pylori (H. pylori) infection has been established as a well-established etiologic agent for gastric cancer (GC) and is a major contributing factor to the worldwide GC-associated mortality. This bacterium colonizes the gastric mucosa and causes chronic inflammation, oxidative stress, and genetic instability that may be responsible for precursor cellular lesions of cancer. These alterations may progress to intestinal metaplasia, atrophic gastritis, and ultimately cancer. Numerous virulence factors, such as Vacuolating Cytotoxin A (VacA) and Cytotoxin-associated gene A (CagA), are also linked to H. pylori. These factors disrupt cellular signaling pathways and prolong inflammation, which in turn promotes carcinogenesis. Environmental factors and host genetic susceptibility also influence how severe H. pylori's effects are. People with underlying genetic susceptibilities or bad habits have an increased risk of complications. Although antibiotic therapies can lower GC risk, antibiotic resistance and reinfection represent quite difficult clinical problems. Because of the close link between H. pylori and GC as well as various other digestive diseases, more active efforts to prevent and treat these diseases should be undertaken.

کلیدواژه ها:

Helicobacter pylori ، Inflammation ، Infection ، gastric ulcer ، oxidative stress