Figure 2.

EGFR signaling in myeloid cells promotes formation of colitis-associated and Apc^Min-driven intestinal tumorigenesis. (A) Hematoxylin-eosin colon staining of AOM/DSS-treated mice. Arrowheads depict tumors. Scale bars 1 mm. (B) Immunofluorescence double staining of EGFR/CD64 on colorectal tumors. Arrowheads depict presence of EGFR⁺/CD64⁺ cells. Scale bars 50 μm. (C) Tumor penetrance in AOM/DSS-treated mice (ctrl [control], n = 10; Egfr^wa2/wa2, n = 5; Egfr^f/f, n = 22; Egfr^ΔIEC and Egfr^ΔMYL, n = 15; Egfr^ΔIEC/ΔMYL, n = 12). *P < .05, **P < .01, Fisher’s exact test. (D–F) Analysis of tumor formation in AOM/DSS-treated mice (see [C] for number of mice). (D) Tumor area, (E) load (tumor area (×10^–2)/colon area), and (F) multiplicity (number of tumors/cm² colon area). (G) Proliferation index (BrdU-incorporated tumor cells/area, 9 tumors from 3 different mice were counted). Data are mean ± SEM. (H) Apoptotic index (cleaved Caspase-3⁺ tumor cells/area, 14–28 tumors from 3–6 different mice were counted). (I–K) Analysis of tumor formation in the Apc^Min background (Apc^Min/+;Egfr^wa2/+, n = 9; Apc^Min/+;Egfr^wa2/wa2, n = 8; Apc^Min/+;Egfr^f/f, n = 18; Apc^Min/+;Egfr^ΔIEC, n = 9; Apc^Min/+;Egfr^ΔMYL, n = 11). (I) Tumor area, (J) load, and (K) multiplicity. Data from (D–K) are mean ± SEM, *P < .05, **P < .01, t test. # P < .05, ## P < .01, 1-way analysis of variance with Dunn’s posttest.