Wound-promoted tumor growth and SDF-1α levels in wound fluid are dependent on the host background.

<p><b>A,B.</b> The host background influenced wound-promoted tumor growth. <b>A.</b> Wound-promoted tumor growth was assessed in female animals of the F1 generation derived from BALB/c mice bred with BALB/c (control), FVB/nJ, AKR/J, C57Bl/6JNcr, DBA/2J animals. <b>B</b>. Cumulative tumor volumes. Unpaired t-test. Mean ±95% CI. Representative of 2 independent experiments is shown. <b>C,D.</b> The host background influences SDF-1α levels in wound fluid. <b>C.</b> SDF-1α levels were analyzed by ELISA in healthy hosts 2 d or 9d after subcutaneous implantation of PVA sponges. <b>D.</b> SDF-1α levels in wound fluid (ELISA). Mann-Whitney test. N.A. : sample number not sufficient to perform statistical analysis. Bar: mean.</p

SDF-1α is elevated in wound fluid and increases tumor growth.

<p><b>A.</b> SDF-1α levels in wound fluid from BALB/c wildtype (WT) mice were higher than in wound fluid from BALB/c nu/nu mice (nu/nu) or plasma from BALB/c WT animals (cytokine microarray). <b>B.</b> SDF-1α levels in wound fluid from BALB/c WT animals increased during the course of wound healing and were higher in WT wound fluid than in wound fluid from nu/nu animals 9d after wounding (insert). n = 5 samples/time point (0.3d to 5d) and n = 3 samples/time point (5d to 14d); Triangle: mean; filled circle: individual data point. Insert: p = 0.05, n = 3, Mann Whitney test). <b>C, D.</b> Inhibition of SDF-1α/CXCR4 signaling by AMD3100 treatment abolished wound-promoted-tumor growth. <b>C.</b> Experimental design. <b>D.</b> Cumulative tumor volumes. p = 0.0027, n = 10 animals/group, Kruskal Wallis Test/Dunn’s Multiple Comparison Test, observation time: 21d, mean ±95% CI.</p