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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Phytosomal curcumin causes natural killer cell-dependent repolarization of glioblastoma (GBM) tumor-associated microglia/macrophages and elimination of GBM and GBM stem cells

Fig. 3

CCP treatment triggers intra-tumor recruitment of peripheral macrophages equally in both CCP and CCP + NK1.1 groups. GBM Brain sections parallel to those used for IHC in Fig. 2 were used to assess the possibility of intra-tumor recruitment of peripheral macrophages (macrophage specific marker RM0029-11H3(+)). a The GBM sections from the Vehicle-treated mice harbored mostly tumor-associated microglia (Iba1(+), RM0029-11H3(−), green) and a few macrophages (Iba1(+), RM0029-11H3(+), yellow) (first row), whereas the CCP (second row) and CCP + NK1.1-treated (third row) mice showed abundant tumor-associated macrophages (Iba1(+), RM0029-11H3(+)). Double-staining (Iba1(+), RM0029-11H3(+)) of peripheral tumors (HPV(+) TC1 tumors) (fourth row) confirmed that the tumor-associated cells observed in the GBM sections were macrophages from the periphery. b CCP-treatment triggered a 53% increase in the number of recruited intra-tumor macrophages (yellow)(*p = 7.8 × 10− 4 Vehicle versus CCP). The CCP + NK1.1 group also showed a 60% increase in the number of recruited intra-GBM macrophages (**p = 3 × 10− 3 Vehicle versus CCP + NK1.1). Three sections per mouse were used for IHC and the data (mean ± S.D.) obtained from Vehicle-treated (n = 4), CCP-treated (n = 4), and CCP + NK1.1-treated mice (n = 4). (Scale bar: 47.62 μm)

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