Role of Helicobacter pylori in Gastric Carcinoma: A Review

Abstract

Gastric cancer (GC) is one of the leading causes of cancer-related deaths globally. Gastritis caused by Helicobacter pylori (H. pylori) is a potent cause of gastrointestinal malignancies. The majority of all humans on the planet have H. pylori invasion in their stomachs, yet only a few diseased people develop GC. The human gastrointestinal system contains a broad population of microorganisms in addition to H. pylori. H. pylori heterogeneity has been studied because not all H. pylori diseases result in cancer. Individuals in the adult age group account for the bulk of gastric carcinoma cases. H. pylori has various strains, which is beneficial for its survival in host cell epithelium for a longer duration of time. Along with H. pylori, oral microbes have a major role in the pathogenicity of gastric carcinoma. The complex ecology of oral microbiota helps to defend against infections, preserve homeostasis, and regulate the immune system. In contrast, oral microbiota is involved in various mechanisms like anti-apoptotic activity, suppression of the immune system of the host, and initiation of chronic inflammation. These oral microbes are also responsible for the development of mutations. Interactions between the host immune system and bacteria promote the progression of cancer. For this review, various research articles were studied, and information was collected using databases like PubMed and Google Scholar. This review emphasizes on the role of H. pylori in gastric carcinoma, its pathogenesis, the role of various virulence factors and risk factors related to it, the role of oral microbiota in gastric carcinoma pathogenesis, diagnostic modalities, treatment options, and preventive measures for gastric carcinoma.