Molecular Mechanism of Gastric Cancer

Dear Colleagues,

Gastric cancer is a major threat to the survival outcome of patients. Both the lack of effective early diagnosis and patients’ resistance to existing treatments result in poor prognosis. Therefore, revealing the malignant transformation mechanism implicated in gastric mucosa is essential to the early prevention and control of gastric cancer. Helicobacter pylori is an important factor causing gastric carcinogenesis, and has been identified as a Class I carcinogen by WHO/IARC. Microorganisms, with their residues and metabolites, can accumulate in and interact with cancer cells and immune cells to form the Tumor Microbial Microenvironment, which can induce the dysregulation of gene expression and cell proliferation via a variety of regulatory mechanisms. Meanwhile, gastric carcinoma cells in the TME can interact with innate immune cells, tumor-related fibroblasts, endothelial cells, pericytes and other non-tumor cells through cytokines to co-evolve and promote gastric carcinogenesis. It is essential to explore the mechanisms implicated in the transformation of malignant gastric mucosa and to detect the novel node molecules and regulatory targets involved in it; this is of great significance for the early diagnosis and treatment of gastric cancer.

Prof. Dr. Jiping Zeng
Guest Editor

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