Inflammation and Gastric Cancer

Abstract

Gastric cancer remains a major killer globally, although its incidence has declined over the past century. It is the fifth most common cancer and the third most common reason for cancer-related deaths worldwide. Gastric cancer is the outcome of a complex interaction between environmental, host genetic, and microbial factors. There is significant evidence supporting the association between chronic inflammation and the onset of cancer. This association is particularly robust for gastrointestinal cancers in which microbial pathogens are responsible for the chronic inflammation that can be a triggering factor for the onset of those cancers. Helicobacter pylori is the most prominent example since it is the most widespread infection, affecting nearly half of the world’s population. It is well-known to be responsible for inducing chronic gastric inflammation progressing to atrophy, metaplasia, dysplasia, and eventually, gastric cancer. This review provides an overview of the association of the factors playing a role in chronic inflammation; the bacterial characteristics which are responsible for the colonization, persistence in the stomach, and triggering of inflammation; the microbiome involved in the chronic inflammation process; and the host factors that have a role in determining whether gastritis progresses to gastric cancer. Understanding these interconnections may improve our ability to prevent gastric cancer development and enhance our understanding of existing cases.

Linking dysbiosis to precancerous stomach through inflammation: Deeper than and beyond imaging

“…Chronic inflammation driven by immune cells is a rather complex process requiring multiple cellular players (e.g., macrophages, lymphocytes) and pivotal regulators, including signaling pathways (e.g., NF-kB, JAK-STAT, TLR, MAPK), growth factors (e.g., VEGF, TGF-ß), as well as inflammatory factors (e.g., cytokines, chemokines), inflammasome, and inflammatory metabolites (e.g., prostaglandins, leukotrienes) , as reviewed by Zhao et al (100). Tumor growth is promoted by an inflammatory response, which in turn is induced by inflammatory mediators that can attract immune cells to the lesion (101). That promotes the perfect conditions for the growth, invasion and metastization of tumor cells, known as the tumor microenvironment (101).…”

“…Tumor growth is promoted by an inflammatory response, which in turn is induced by inflammatory mediators that can attract immune cells to the lesion (101). That promotes the perfect conditions for the growth, invasion and metastization of tumor cells, known as the tumor microenvironment (101).…”

Relationship of FDG Uptake of the Reticuloendothelial System with Tumor Immune Microenvironment and Prognosis in Patients with Gastric Cancer

“…In recent decades, several studies have demonstrated that inflammation can involve every process of tumor development, progression, metastasis, and treatment resistance, suggesting that inflammation is one of the hallmarks of cancer [ 1 , 2 , 3 ]. Due to of the notable association of gastric carcinogenesis with Helicobacter pylori infection and Epstein–Barr virus infection, gastric cancer has been considered to be closely associated with infection and chronic inflammation [ 4 ]. In clinical studies of gastric cancer patients, serum inflammatory markers such as C-reactive protein, the neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR), which can reflect the degree of host inflammatory response, were found to be significant predictors of cancer progression and survival [ 5 , 6 ].…”

Impact of interaction between interleukin-6 gene polymorphism and Helicobacter pylori infection on susceptibility to gastric cancer

“…Previous studies (Machlowska et al , 2020) have reported that multiple risk factors can affect the occurrence and development of GC, including Helicobacter pylori (H. pylori ) infection, obesity, current alcohol consumption, current smoking, and excessive sodium intake. In addition, inflammation is also an important factor in the development of GC, and genetic factors involved in inflammation may play an important role in the development of GC (Ji et al , 2021; Jaroenlapnopparat et al , 2022).…”