Abstract
Gastric cancer (GC) is a highly heterogeneous tumor, and TME plays a key role in tumorigenesis and progression. TME is composed of immune cells, CAF and ECM, which regulate the growth, invasion and metastasis of GC through complex interactions. Immune escape mechanisms, such as the activation of the PD-1/PD-L1 pathway, weaken the body's anti-tumor immune response and lead to further proliferation of tumor cells. In addition, high density of immunosuppressive cells and active CAF are strongly associated with poor prognosis in patients with GC. In recent years, targeted therapeutic strategies for TME, such as immune checkpoint inhibitors (ICIs), CAF inhibitors, and ECM remodeling modulators, have shown potential therapeutic effects and become a new way to improve the survival rate of GC patients. However, due to the complexity and heterogeneity of TME, future studies still need to further explore the specific mechanism of action of TME in different stages of GC, and develop more accurate personalized treatment plans. Multidisciplinary combined treatment strategies are expected to play an important role in improving the prognosis of patients with GC.
Published Version
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