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Updated: Jun 7, 2025

Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
Published on: January 22, 2018
Molecular Mechanism for Malignant Progression of Gastric Cancer Within the Tumor Microenvironment
Tasuku Matsuoka1,2, Masakazu Yashiro1,2
1Department of Molecular Oncology and Therapeutics, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 5458585, Japan.
Abstract:
Gastric cancer (GC) is one of the most common cancers worldwide. Most patients are diagnosed at the progressive stage of GC, and progress in the development of effective anti-GC drugs has been insufficient. The tumor microenvironment (TME) regulates various functions of tumor cells, and interactions between the cellular and molecular components of the TME-e.g., inflammatory cells, fibroblasts, vasculature cells, and innate and adaptive immune cells-promote the aggressiveness of cancer cells and dissemination to distant organs. This review summarizes the roles of various TME cells and molecules in regulating the malignant progression and metastasis of GC. We also address the important roles of signaling pathways in mediating the interaction between cancer cells and the different components of the GC TME. Finally, we discuss the implications of these molecular mechanisms for developing novel and effective therapies targeting molecular and cellular components of the GC TME to control the malignant progression of GC.
Insights
Gastric cancer progression is driven by the tumor microenvironment (TME). Targeting TME cells and signaling pathways offers new therapeutic strategies for gastric cancer (GC).
Area of Science:
- Oncology
- Cancer Biology
- Immunology
Background:
- Gastric cancer (GC) is a prevalent global malignancy.
- Late-stage diagnosis limits effective treatment options for GC.
- The tumor microenvironment (TME) significantly influences GC progression and metastasis.
Purpose of the Study:
- To review the role of TME cells and molecules in GC progression and metastasis.
- To examine signaling pathways mediating cancer cell-TME interactions in GC.
- To discuss therapeutic implications for targeting the GC TME.
Main Methods:
- Literature review of TME components in gastric cancer.
- Analysis of cellular and molecular interactions within the GC TME.
- Synthesis of current understanding of GC TME-driven malignancy.
Main Results:
- TME cells (inflammatory, immune, fibroblasts, vasculature) promote GC aggressiveness and metastasis.
- Signaling pathways are crucial for cancer cell communication with the GC TME.
- Understanding these interactions is key to developing targeted therapies.
Conclusions:
- The TME is a critical regulator of gastric cancer malignant progression.
- Targeting specific TME components and pathways holds promise for novel GC therapies.
- Further research into GC TME mechanisms can lead to improved patient outcomes.
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