Figure 3. CXCR2 deficiency suppresses DMBA/TPA skin carcinogenesis.

(A–C) WT and Cxcr2^–/– Balb/c mice received DMBA once, followed 1 week later by 20 weeks of TPA treatment (3 times per week). Number of papillomas/mouse (A; mean ± SEM) and papilloma incidence (B) were recorded weekly. Tumors were measured at the end of the experiment (C). Data were analyzed by Mann-Whitney test (A at week 22 and C) and log-rank analysis with censoring (B). **P < 0.01. (D) Representative sections of anti-MPO–immunostained (brown) WT and Cxcr2^–/– Balb/c DMBA/TPA-induced papillomas. Sections were counterstained with hematoxylin and visualized by light microscopy. Boxed regions are shown at higher magnification in the insets. Scale bars: 200 μm; 50 μm (insets). (E) Average number of MPO⁺ cells per high-powered field (HPF) of 6 papillomas taken from 4 or more mice of each genotype. ***P < 0.001, Mann-Whitney test. (F) Microvessel density in WT and Cxcr2^–/– papillomas (n = 5–6 per group). *P < 0.05, Mann-Whitney test. Box and whisker plots show median (lines within boxes), interquartile range (bounds of boxes), and upper and lower range (whiskers).