Role of the tumor microenvironment in the pathogenesis of gastric carcinoma

Abstract

Gastric carcinoma (GC) is the 4^th most prevalent cancer and has the 2^nd highest cancer-related mortality rate worldwide. Despite the incidence of GC has decreased over the past few decades, it is still a serious health problem. Chronic inflammatory status of the stomach, caused by the infection of Helicobacter pylori (H. pylori) and through the production of inflammatory mediators within the parenchyma is suspected to play an important role in the initiation and progression of GC. In this review, the correlation between chronic inflammation and H. pylori infection as an important factor for the development of GC will be discussed. Major components, including tumor-associated macrophages, lymphocytes, cancer-associated fibroblasts, angiogenic factors, cytokines, and chemokines of GC microenvironment and their mechanism of action on signaling pathways will also be discussed. Increasing our understanding of how the components of the tumor microenviroment interact with GC cells and the signaling pathways involved could help identify new therapeutic and chemopreventive targets.

Keywords: Tumor microenvironment; Gastric carcinoma; Inflammation; Helicobacter pylori; Cytokine

Core tip: The intensive interplay that exists between tumor cells and the tumor microenvironment can play an important role in tumor initiation, growth and metastasis. A better understanding of the molecular pathogenesis of the tumor microenvironment of Gastric carcinoma would be crucial for the design of novel molecular targets. In this review, we have provided an overview of the currently available knowledge of the role of the TME in gastric cancer and have highlighted the potential prognostic and therapeutic implications.