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Additional file 1: Fig. S1. Relatively lower dose of Lentinan (LNT) treatments inhibited EO771-L1 breast tumor growth. (a) Experimental design: C57BL/6 mice were subcutaneously (s.c.) inoculated with 2×105 EO771-L1 breast cancer cells on the right flank. When tumors reached 3×4 mm in diameter, mice were randomly divided into 5 groups and received i.p. injection of different doses of LNT (0.5 mg/kg, 1.0 mg/kg, 2.0 mg/kg, 4.0 mg/kg) daily for 9 days; (b) Tumor growth curves were recorded and tumor volume was calculated at the end of the treatments; NS: control group treated with saline. All data in this report are presented as means ± SEM. * p< 0.05. Fig. S2. LNT (1 mg/kg, every other day) treatments inhibited EO771-L1 breast tumor growth. (a) Experimental design: C57BL/6 mice were s.c. inoculated with 2×105 EO771-L1 breast cancer cells on the right flank. When tumors reached 3×4 mm in diameter, mice were received different doses of LNT (0. 5 mg/kg, 1.0 mg/kg, 2.0 mg/kg) treatments, every other day, for 9 days; (b) Tumor growth curves were recorded and tumor weight was measured at the end of the treatments. NS: control group treated with saline. All data in this report are presented as means ± SEM. * p< 0.05, ** p< 0.01, *** p< 0.001. Fig. S3. The gating strategy to analyze intratumoral CD4+ and CD8+ T cells in EO771 breast tumor model. Fig. S4. The effects of LNT treatments on intratumoral macrophages and neutrophils in EO771-R1 and EO771-L1 breast tumors. (a) The representative flow figures of myeloid cells; (b) The proportions of TAMs and neutrophils. All data in this report are presented as means ± SEM. ** p< 0.01. Fig. S5. The combination of LNT treatments and DLL1 overexpression synergistically inhibited LAP0279 lung cancer growth. (a) Experimental design: FVB mice were s.c. inoculated with 2×105 LAP-R1 or LAP-L1 lung cancer cells on the right flank. When tumors reached 5×6 mm in diameter, mice were randomly divided into 4 groups and received i.p. injection of saline or 1.0 mg/kg LNT every other day for two doses; (b) Tumor growth curves were recorded and tumor weight was measured at the end of the treatments. NS: control group treated with saline. All data in this report are presented as means ± SEM. ** p< 0.01, *** p< 0.001. Fig. S6. The gating strategy to analyze intratumoral CD4+ T cells, CD8+ T cells, neutrophils and macrophages in LAP0297 lung tumor model. Fig. S7. LNT treatments increased the proportions of effector CD8+ T cells in LAP lung tumors. (a) The representative flow figures of CD8+CD44+CD69- and CD8+CD44+CD69+ T cells in LAP-L1 lung tumors; (b) The proportions of intratumoral CD8+CD44+CD69- and CD8+CD44+CD69+ T cells in LAP-L1 lung tumors. All data in this report are presented as means ± SEM. * p< 0.05, ** p< 0.01, *** p< 0.001. Fig. S8. LNT treatments increased the proportions of central memory CD8+ T cells in LAP lung tumors. (a) The representative flow figures of CD8+CD44+CD62L- and CD8+CD44+CD62L+ T cells in LAP-L1 lung tumors; (b) The proportions of intratumoral CD8+CD44+CD62L- and CD8+CD44+CD62L+ T cells in LAP-L1 lung tumors. All data in this report are presented as means ± SEM. * p< 0.05, *** p< 0.001. Fig. S9. The improved antitumor effects of LNT in LAP-R1 lung cancers were dependent on intratumoral CD11b+Gr1hi neutrophils. (a) Experimental design: FVB mice were s.c. inoculated with 2×105 LAP-R1 lung cancer cells on the right flank. When tumors reached 5×6 mm in diameter, mice were randomly divided into 4 groups and received i.p. injection of NS (saline), LNT (1.0 mg/kg), anti-Gr1 antibody (200 μg/mouse) or LNT plus anti-Gr1 antibody for 9 days; (b) Tumor growth curves were recorded and tumor weight was measured at the end of the treatments; (c) The proportions of TAMs; (d) The proportions of intratumoral Gr1hiCD11b+ (CD11b+Ly6G+) neutrophils. All data in this report are presented as means ± SEM. * p< 0.05,** p< 0.01, *** p< 0.001. Fig. S10. The gating strategy to analyze intratumoral neutrophils and macrophages in LAP0297 lung tumor model.