Cetuximab inhibits Schwann cell EGFR phosphorylation and proliferation. Newborn CNPase-hEGFR mice were treated with cetuximab from birth to 2 weeks of age, and nerves were stained with antibodies specific to phospho-EGFR or BrdU. A: Untreated CNPase-hEGFR nerve stained with an antibody specific to phospho-EGFR (green). Nuclei are counterstained with DAPI (red). B: CNPase-hEGFR nerve treated with cetuximab (0 × 2) showed decrease in level of phospho-EGFR (green). C–G: BrdU staining of sciatic nerve tissue sections. Nuclei are counterstained with DAPI (blue). C: WT nerve contained low levels of BrdU(+) cells (red). D: CNPase-hEGFR nerve contained high levels of BrdU(+) cells (red). E: CNPase-hEGFR nerve from mice treated with cetuximab (0 × 2) showed BrdU(+) cell numbers restored to WT levels (red). F: Bar graph shows quantification of percentage of cells BrdU(+). Positive nuclei were quantified from control or cetuximab-treated (0 × 2) CNPase-hEGFR mouse nerves (black bars) or WT counterparts (white bars). Percentage of BrdU(+) cells was significantly higher in untreated CNPase-hEGFR nerves compared to WT (P < 0.001, n = 4). Percentage of BrdU(+) cells was not significantly different between WT and cetuximab-treated CNPase-hEGFR nerves (P = 0.30, n = 4). G: Quantification of total nuclei number per high-powered fields from control or cetuximab-treated (0 × 2) CNPase-hEGFR mouse nerves (black bars) or WT counterparts (white bars). Nuclei number was significantly higher in untreated CNPase-hEGFR nerves compared to WT (P < 0.0001, n = 4). Nuclei number was not significantly different between WT and cetuximab-treated CNPase-hEGFR nerves (P = 0.34, n = 4). Scale bars, 20 μm.