Abstract:
Gastric cancer is one of the most common and deadliest cancers in the world. Patients face a 25% five-year survival rate and diagnosis is often delayed as gastric cancer typically presents as asymptomatic or with nonspecific symptoms2. There are many environmental, epigenetic, and genetic factors involved in the initiation and progression of gastric cancer. Helicobacter Pylori is a pathogenic bacterium that colonizes the stomach mucosa and is the strongest known environmental risk factor for gastric cancer. H. pylori is classified as a type I carcinogen, causing inflammation, and increasing the risk of gastric cancer. However, the mechanisms of H. pylori mediated gastric tumorigenesis are poorly understood. Immune cells during infection and disease can release inflammatory mediators such as chemokines and cytokines that can exhibit antitumorigenic or pro-tumorigenic capabilities. Chronic inflammation stimulated by H. pylori infection can trigger innate and adaptive immune responses3. Recently, activated eosinophils were found to accumulate in the gastric mucosa upon H. pylori infection, and the number of infiltrating eosinophils increases as disease progresses1. Unresolved immune responses can trigger chronic inflammation and promote cancer growth. Therefore, I hypothesize that H. Pylori promotes gastric tumorigenesis through the modulation of eosinophils. To address this hypothesis, I will use an H. pylori infection in vitro and in vivo models to examine the role eosinophils play in regeneration and tumorigenesis.
