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World J Clin Oncol. May 24, 2026; 17(5): 119163
Published online May 24, 2026. doi: 10.5306/wjco.v17.i5.119163
Figure 1
Figure 1 Shilajit and glycine-induced apoptosis in breast and liver cancer cells.
Figure 2
Figure 2 Immune cells in the tumor microenvironment. NKM1: Natural killer cell, type 1; Th1: T helper cell, type 1; ILC1: Group 1 innate lymphoid cell; IFN: Interferon; TNF: Tumor necrosis factor; DC: Dendritic cell; N1: Neutrophil, type 1; M1: Macrophage, type 1; MDSC: Myeloid-derived suppressor cell; IL: Interleukin; CCL: CC chemokine ligand; TGF: Transforming growth factor.
Figure 3
Figure 3 Molecular mechanisms of shilajit in cancer modulation. Bax: B-cell lymphoma/Leukemia-2 family-associated X protein; Bcl-2: B-cell lymphoma/Leukemia-2 family; NF-κB: Nuclear factor-kappa B; VEGF: Vascular endothelial growth factor.
Figure 4
Figure 4 Glycine’s roles in redox balance, cytoprotection, and immune regulation. NF-κB: Nuclear factor-kappa B; Th1/2: T helper cell, type 1/2; IL: Interleukin.
Figure 5
Figure 5 Comparative and overlapping mechanisms of shilajit and glycine in cancer modulation. MDSC: Myeloid-derived suppressor cell; Bcl-2: B-cell lymphoma/Leukemia-2 family.
Figure 6
Figure 6 Integrative mechanisms of shilajit and glycine in cancer therapy. NF-κB: Nuclear factor-kappa B; VEGF: Vascular endothelial growth factor; STAT3: Signal transducer and activator of transcription 3; MDSC: Myeloid-derived suppressor cell; ROS: Reactive oxygen species.


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