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About the Authors:
Dun-Fa Peng
Affiliation: Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America
Tian-Ling Hu
Affiliation: Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America
Barbara G. Schneider
Affiliation: Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America
Zheng Chen
Affiliations Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, Department of General Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China
Ze-Kuan Xu
Affiliations Department of General Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China, Institute of Tumor Biology, Jiangsu Province Academy of Clinical Medicine, Nanjing, China
Wael El-Rifai
* E-mail: [email protected]
Affiliations Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, Department of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, Department of Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee, United States of America
Introduction
Gastric cancer (GC) is the fourth most common cancer in the world [1], [2] with about 900,000 new cases diagnosed in the world each year [2]. Gastric cancer remains the second leading cause of cancer-related deaths worldwide [2]. Although there has been a decline in the overall incidence of distal gastric cancer during the past decades, the incidence is rising for adenocarcinomas of the proximal part of the stomach in the Western world [2]. It is generally agreed that gastric cancer is a multifactor disease in which Helicobacter pylori (H. pylori) infection plays a crucial role, especially for distal gastric cancer [3]–[5]. Accumulating data indicate that H. pylori infection generates high levels of reactive oxygen species (ROS) from multiple sources [6]. Activated neutrophils, for example, are the main source of ROS production in the H. pylori-infected stomach; however, H. pylori itself can also produce ROS [7]. In addition, extensive recent studies have revealed that H. pylori-induced ROS production in gastric epithelial cells might affect gastric epithelial cell signal transduction, resulting in gastric carcinogenesis [8]–[10]. Excessive ROS production in the stomach promotes DNA damage in gastric epithelial cells, suggesting its involvement in gastric carcinogenesis [7], [11], [12].
Normal cells have intact antioxidative properties that protect cells from ROS-induced DNA damage and cell injury [13]–[15]. Among these systems,...