Activated EGFR (red) and Ki67 (green) were expressed abundantly in head and neck carcinoma xenografts developed in nude mice. Cetuximab treatment caused more prolonged inhibition of EGFR, its downstream effectors STAT3 and Bcl_XL, and the proliferation marker Ki67 compared with treatment with gefitinib. This resulted in a more potent tumor response to cetuximab compared with gefitinib in this model system. For further details, please see Feng et al. on page 2512 in this issue.

[Table of Contents]