<i>Helicobacter pylori</i> Oncogenicity: Mechanism, Prevention, and Risk Factors
Muzaheed Muzaheed
Abstract
Helicobacter pylori ( H . pylori ) is the most common cause of gastric ulcer; however, its association with gastric cancer has been proved through a variety of studies. Importantly, H . pylori infection affects around half of the world’s population leading to a variety of gastric problems and is mostly present in asymptomatic form. Although about 20% of people infected with H . pylori develop preneoplastic gastric lesions in later stages of their life, around 2% of infected individuals develop gastric cancer. Nevertheless, the outcome of H . pylori infection is determined by complex interaction between the host genetics, its environment, and virulence factors of infecting strain. There are several biomarkers/traits of H . pylori that have been linked with the onset of cancer. Among these, presence of certain major virulence factors including cytotoxin-associated gene A (CagA), vacuolating cytotoxin (VacA), and outer inflammatory protein A (OipA) plays a significant role in triggering gastric cancer. These factors of H . pylori make it a potent carcinogen. Therefore, eradication of H . pylori infection has shown positive effects on decreasing the risk of gastric cancer, but this has become a challenge due to the development of antibiotic resistance in H . pylori against the antibiotics of choice. Thus, the unmet need is to develop new and effective treatments for H . pylori infection, considering the antimicrobial resistance in different regions of the world. This review discusses the properties of H . pylori associated with increased risk of gastric cancer, antibiotic resistance pattern, and the possible role of eradication of H . pylori in preventing gastric cancer.