Helicobacter pylori Infection and Dietary Factors Act Synergistically to Promote Gastric Cancer.

Negin Raei,Bahador Behrouz,Saber Zahri,Saeid Latifi-Navid

doi:10.7314/apjcp.2016.17.3.917

Abstract

However, the incidence of gastric cancer (GC) has been decreased in past decades; GC is the second cause of cancer related death in the world. Evidence has illustrated that several factors including Helicobacter pylori (H. pylori) infection, host genetics, and environmental factors (smoking and particularly diet) may play a crucial role in gastric carcinogenesis. It has been demonstrated that high consumption of fresh fruits, vegetables, high level of selenium and zinc in drinking water, sufficient iron, and cholesterol protect against GC, while; smoked , pickled, and preserved foods in salt, and nitrites increase the risk of GC. Epidemiological studies have also proved that H. pylori infection and a high salt diet could independently induce atrophic gastritis and intestinal metaplasia. Recently, studies have been demonstrated that dietary factors directly influence H. pylori virulence. The use of appropriate diet could reduce levels of H. pylori colonization or virulence and prevent or delay development of peptic ulcers or gastric carcinoma. This is attractive from a number of perspectives including those of cost, treatment tolerability, and cultural acceptability. This review will describe new insights into the pathogenesis of H. pylori in relation to environmental factors, especially dietary, not only to find the developed means for preventing and treating GC, but also for understanding the role of chronic inflammation in the development of other malignancies.

Highlights

The incidence of gastric cancer (GC) has been declined over time, but it is the second cause of death from cancer in the world (Jemal et al, 2011; de Martel et al, 2012; Cover and Peek, 2013; Ferlay et al, 2013; Epplein et al, 2014)
Evidence has illustrated that several factors including Helicobacter pylori (H. pylori) infection, host genetics, and environmental factors may play a crucial role in gastric carcinogenesis
Diet has long been thought to be correlated with GC risk, most of the published studies have been reported that there is a synergistic interaction between the dietary factors and the H. pylori infection in relation to GC risk (Yamaguchi and Kakizoe, 2001)

Summary

Introduction

The incidence of gastric cancer (GC) has been declined over time, but it is the second cause of death from cancer in the world (Jemal et al, 2011; de Martel et al, 2012; Cover and Peek, 2013; Ferlay et al, 2013; Epplein et al, 2014). Non-phosphorylated cagA manipulates PAR1b and promotes loss of cell polarity It interacts with the epithelial tight-junction scaffolding protein ZO-1 and the transmembrane protein junctional adhesion molecule-A (JAM-A) resulting in aberrations in tight junction function at bacterial adherence site (Amieva et al, 2003), and activates β-catenin which upregulates the genes which are involved in cancer progression (Franco et al, 2005). Due to the mentioned activities cagA has been known as bacterial oncoprotein (Murata-Kamiya et al, 2007) Another H. pylori virulence factor that is associated with the development of GC is the secreted vacuolating cytotoxin A (VacA) toxin (Cover and Blanke, 2005; Boquet and Ricci, 2012). Patients infected with H. pylori harboring cag PAI are at high risk of GC (Cover and Peek, 2013)

Environmental Factors and GC Risk

Dietary Risk Factors for GC

Other Risk Factors

Findings

Conclusion