In this issue of Cancer Cell, Mellinghoff et al. (2004) demonstrate that a small molecule inhibitor of the EGF receptor (EGFR) and the HER2/ErbB2/c-Neu kinase blocks signaling to the androgen receptor by a mechanism that involves HER2/HER3 heterodimerization. Surprisingly, the EGFR is peripheral to this signaling mechanism. These results have implications for the design of targeted therapy for hormone-refractory prostate cancer.
