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. 2012 Mar 12;209(3):495–506. doi: 10.1084/jem.20111413

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© 2012 Scarlett et al.

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Figure 4. — A change in the inflammatory microenvironment converges with the exponential growth of p53/K-ras tumors. (A) Top, images of explanted reproductive organs from p53/K-ras mice after receiving adenovirus. Middle and bottom, quantified flow analysis of resected tumors (red circle; primordial and advanced) from p53/K-ras (middle; n = 4–6) and WT (bottom; n = 6–8) animals, which received adenovirus previously. Slices represent mean percentages of CD45⁺ leukocytic infiltrates. (B) Comparative analysis of CD45⁺CD11c⁺CD11b⁻ and CD45⁺CD3⁺ cells infiltrating tumors of p53/K-ras mice at the indicated time points (n = 4–8). (C) Density plots of p53/K-ras tumors or WT ovaries which received adenovirus 35 d before (gated on CD45⁺ cells). Histogram of CD45⁺F4/80⁺CD11c⁻ (blue) and CD45⁺CD11c⁺F4/80⁻ (red). Numbers in the right corner are respective mean fluorescence intensity (MFI). (D) Percentage of CD45⁺CD11c⁺ and CD45⁺CD3⁺ cells found within stage III/IV human ovarian carcinoma (n = 7). (E and F) Quantification of flow analysis at the indicated time points of ovaries from p53/K-ras (n = 4–6) or WT (n = 6–8) mice after adenovirus injection. Error bars, SEM. *, P < 0.05; **, P < 0.001; ***, P < 0.0001; ns, no significance).