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Copyright ©The Author(s) 2024.
World J Gastrointest Oncol. Jul 15, 2024; 16(7): 2915-2924
Published online Jul 15, 2024. doi: 10.4251/wjgo.v16.i7.2915
Figure 1
Figure 1 Tumor-associated macrophages have dual potential in the tumor microenvironment. TME: Tumor microenvironment.
Figure 2
Figure 2 Tumor-associated macrophages can promote tumor cell progression through a variety of pathways. CCL: CC ligand; CXCL: CXC ligand; miRNA: MicroRNA; ncRNA: Non-coding RNA; TAM: Tumor-associated macrophage.
Figure 3
Figure 3 Low expression of secreted protein acidic and rich in cysteine 1 in gastrointestinal stromal tumor promotes the proliferation of blood vessels and tumor cells. CCL: CC ligand; GIST: Gastrointestinal stromal tumor; SPARCL1: Secreted protein acidic and rich in cysteine 1.
Figure 4
Figure 4 Imatinib combined with anti-programmed death receptor-1/programmed death ligand-1 therapy can inhibit M2 polarization of tumor-associated macrophages. IDO: 2,3-dioxygenase; IFN: Interferon; IL: Interleukin; PD-1/PD-L1: Programmed death receptor-1/programmed death ligand-1; TGF: Transforming growth factor; TNF: Tumor necrosis factor.
Figure 5
Figure 5 Inhibiting the generation of M2 tumor-associated macrophages is important for tumor progression. GIST: Gastrointestinal stromal tumor; IFN: Interferon; IL: Interleukin; PD-1/PD-L1: Programmed death receptor-1/programmed death ligand-1; TGF: Transforming growth factor.