Intersections between innate immune response and gastric cancer development

Area of Science:

• Oncology
• Immunology
• Gastroenterology

Background:

• Gastric cancer (GC) remains a significant global health challenge, ranking as the fifth most diagnosed malignancy and fourth leading cause of cancer-related deaths.
• High mortality rates are observed in Asian and Latin American regions, often due to late-stage diagnosis.
• GC development is multifactorial, involving Helicobacter pylori (H. pylori) virulence, environmental factors, diet, and host genetics, with a chronically inflamed tumor microenvironment promoting progression.

Purpose of the Study:

• To review the role of innate immune activation in gastric cancer.
• To explore the involvement of innate immunity in premalignant gastric lesions and established tumors.
• To highlight the importance of assessing inflammation in GC for therapeutic strategies.

Main Methods:

• Literature review focusing on innate immunity, inflammation, and gastric cancer.
• Analysis of molecular mechanisms including Toll-like receptors, cytokines, and NETosis.
• Examination of H. pylori's role and host-pathogen interactions in gastric tumorigenesis.

Main Results:

• Innate immune responses, mediated by Toll-like receptors and cytokines, are implicated in GC development.
• Chronic inflammation and H. pylori infection create a tumor microenvironment that favors cancer progression.
• Immune checkpoint molecules, interferon-gamma pathway, and NETosis are associated with increased GC risk.

Conclusions:

• Innate immune activation is a critical component of gastric cancer pathogenesis.
• Comprehensive assessment of inflammation, including H. pylori status, is necessary for understanding GC.
• Further research into innate immunity pathways may reveal novel therapeutic targets for gastric cancer.