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The Science Journal of the Lander College of Arts and Sciences

Authors

Chaya S. Lowy

Abstract

Gastric cancer is a major public health concern due to the many deaths it is associated with. H. pylori is present in almost all gastric cancer patients; thus, it is fundamental to understand how H. pylori is implicated in the etiology of gastric cancer. The research in this paper is primarily based on studies acquired from Touro College Online Libraries. The bacteria have the means to survive the harsh environment of the stomach by creating a safe microenvironment and propelling themselves toward safer territory. If the bacteria attach to host cells, H. pylori injects cytotoxin-associated protein A (CagA) and vacuolating cytotoxin A (VacA) into their host, inducing inflammation and disrupting cell functions. H. pylori continues to survive at the surface epithelia through various functions and causes damage to epithelial cells. Following gastritis, ulceration or gastric cancer may develop. Mechanisms of the proliferation of cells are abundant but stem from the destruction of cells due to inflammation. The prognosis of gastric cancer is poor due to the advanced stage of cancer at the time of detection. Surgical removal of the tumor, although sometimes employed, is not always recommended or successful. Since a large majority of individuals are infected with non-pathogenic strains of H. pylori, treatment isn’t always suggested. Moreover, some research suggests that there are benefits to being infected with H. pylori.

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