Publications

Abstract

Endocrine resistance is a major limitation to the successful treatment of estrogen receptor-positive (ER+) breast cancer and the EGFR and ErbB2 receptor tyrosine kinases are involved in this process. A recent study now implicates the other 2 ErbB family members, ErbB-3 and -4. Exposure of ER+ breast cancer cells to the pure antiestrogen, fulvestrant, increased levels of ErbB-3 or ErbB-4 and sensitivity to the growth stimulatory effects of heregulin ?1, a potent ligand for these receptors. Thus, the initial growth inhibitory effects of fulvestrant appear compromised by cellular plasticity that allows rapid compensatory growth stimulation via ErbB3/4. Further evaluation of pan-erbB receptor inhibitors in endocrine resistant disease appears warranted.