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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: NK cell-triggered CCL5/IFNγ-CXCL9/10 axis underlies the clinical efficacy of neoadjuvant anti-HER2 antibodies in breast cancer

Fig. 3

NK cell and anti-HER2 antibody combined treatment in a humanized mice model of HER2-positive breast cancer. HCC1954 cells (4 × 105) were subcutaneously implanted in NSG mice. When tumors reached 100 mm3 mice were treated with either: i) isotype control (rituximab; 2 mg/Kg intraperitoneal); ii) trastuzumab (Tz)/pertuzumab (Pt) (1 mg/Kg each, intraperitoneal); iii) expanded human NK cells (2.5 × 106, intratumoral); or iv) trastuzumab/pertuzumab in combination with expanded human NK cells. Mice were sacrificed at the end of treatment. Remnant tumors were excised and processed for RNA extraction and immunostaining of tumor-infiltrating NK cells as indicated in methods. A Treatment schedule. B Tumor volume fold change in each treatment group (n = 5 mice/group). Statistical significance by two-way ANOVA test. C CCL5, IFNG, CXCL9 and CXCL10 expression by RT-qPCR in total tumor RNA extracts in each treatment group. D CD16 and CD103 surface expression in expanded NK cells prior to intratumoral injection (eNK; pre) as well as in tumor-infiltrating NK cells (TI-NK) for the indicated treatment groups

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